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We understand the importance of your wellness. To achieve your wellness objectives, you have come to expect the highest levels of service and patient care. As a result, we continuously commit ourselves to meeting and exceeding your expectations. To us, providing a total healthcare experience means dedicated and friendly staff, flexible and convenient hours, and the highest quality care available.

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At the Center for Personalized Medicine we specialize in prescription natural hormone replacement for both women and men. We can also customize a vitamin program for you. Your nutritional needs are as unique to you as your fingerprint.

At the Center for Personalized Medicine we can also help your memory stay sharp, help your skin stay more youthful, and show you safe and simple ways to increase your growth hormone level. We also have nurses and nutritionists who will meet with you to develop your own individualized weight management program to help you achieve maximum weight loss and keep the weight off.

Have our doctors show you how to lower cholesterol without a prescription. We help cancer patients with nutritional support. If you have diabetes, let us show you new treatment options. In short, at the Center for Personalized Medicine we will take a functional medicine approach to your health care needs.

Whether you want to maintain your current good health, or if you have a disease, we will look at how your body works and design a treatment plan for you and you only. We do not mask your symptoms with medications, we instead try to fix the cause of the problem and use medications only when necessary.

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[Note from Editor: The Grand Master of Chinese Medicine is an honorary title granted by Chinese government, and selected by a panel of various experts. The first selection occurred in 2008-09 and 30 TCM experts were named the Master of Chinese Medicine in 2009. The selection will take place every 5 years. Here are some secrets of longevity from 10 of the 30 Grand Masters. For more information about them, go to: http://baike.baidu.com/view/2411533.htm%5D

Tietao Deng

Tietao Deng, 95 years old, tenured professor of Guangzhou University of Chinese Medicine. , 95)

1. Dont compete for fame, and let nature take its course; 2. Adjust diet and lead a regular life. 3. Do regular exercise, do Eight Pieces of Brocade every morning. He suggested, I have a secret bath prescription. Alternate hot and cold bath and they are relatively cold and hot alternation, which will make the blood vessels contraction and relaxation just like massaging the vessels.

Liangchun zhu

Liangchun Zhu, 94 years old, a famous TCM doctor in Jiangsu Province, he is an expert of TCM for cancer treatment ,94)

Since a long time ago Dr. Zhu eats a special kind of Yang Sheng congee, made by green been 50g, pearl barley 50g, lotus seed 50g, lentils 50g, dates 30g, lycium barbarum (goji berries) 10g, astragalus membranaceus 250g ( 30g for regular persons daily). Wash the first 5 and put them into a boiling casserole and add the water from astragalus membranaceus. Cook on high flame until it boils then change to low flame for 40 min. Then add goji berries into it and continue for 10 more min. Have 1/5 of the amount daily -dividing the dosage into taking half of it before breakfast and the other half after dinner.

Dexin Yan, 91 years old, the leader of Chinese Medicine in Shanghai, the master of balancing Qi and blood. , 91)

Dexin Yan

Longevity and aging are closely related to qi and blood balance. Smooth qi and Blood circulate the whole body and adjust the functions of internal organs to promote longevity. The main supplements I have are some Chinese herbals for Spleen, adding qi and increasing Blood circulation including red flowers, walnuts and so on. I suggest taking these herbals with water and empty stomach only once every morning not twice per day.

Guangxin Lu, 84 years old, Professor at Chinese Academy of Chinese Medicine, expert in TCM theory; , 84)Dr. Lu advises chewing and swallowing slowly, it may take a while for him to eat just an

Guangxin Lu

egg. Dr. Lu always says Eating should be with an enjoyable attitude. He eats 2 eggs every day and he believes that eggs contain a lot of lecithin which helps fight against aging. Getting up early every day, he rubs his ears and belly to make meridian vessels and blood circulates well. In addition, a foot bath before going to bed will let you sleep better.

Zhizheng Lu

Zhizheng Lu, 91 years old, a famous TCM doctor in Beijing; ,91)

Dr. Lu eats ginger after getting up in the morning. He believes eating ginger with dates and brown sugar promotes health and wellbeing. However, he advises only to eat ginger in the morning but not at night. Dr. Lu is in the habit of massaging and rubbing his face in the morning and having a foot bath before going to bed. The foot bath will pull the blood down and it is assists the brain in getting into sleep mode.

Zhongying Zhou

Zhongying Zhou, 84 years old, former president of Nanjing University of Chinese Medicine; ,84)

Dr. Zhou sees patients for 5 half-days every week. It is his greatest pleasure to see and help patients. His lifestyle and routine is very regular, and he never stays up late at night. Desire is the source of suffering; less desire leads to stronger mind. People should live with low-desire, and with a lot of calmness and tolerance.

Youzhi Tang, 85 years old, worked for Chairman Mao as a TCM doctor; ,85)

According to Dr. Tang, the secrets of longevity are: A nurturing life needs a nurturing mind; an open mind leads to happiness. Keep a hospitable and peaceful mind. He sees patients in clinic twice a week and is willing to accept new things. He enjoys thinking which keeps the brain working. In addition, he recommends making sure you have enough sleep, at least 7 hours a day, and take time for a lunch nap.

Zhenghua Li, 87 years old, the former president of Henan College of Chinese Medicine. ,87)

Zhenghua Li

Dr. Li practiced Chinese medicine for more than 60 years. He emphasizes nourishing the Stomach and Spleen, adjusting diet and never engaging in binge eating. He recommends paying attention to exercise and taking a walk after a meal. He walks in the living room for 15 min in the winter when he cant go outside. He writes in calligraphy (handwriting with special pen) to nurture life and taking care of the temperament.

Qi Zhang

Qi Zhang, 90 years old, chief expert of Chinese medicine on kidney diseases, , 90)

Dr. Zhang longevity secrets are keeping your spiritual aspect pleasurable and free from worry and anxiety. Ignore rumors and burdens that make you unhappy, instead just laugh at them. Eating and diets should follow the natural way, neither eating too much nor eating to light. He prefers a balanced diet and does not agree with avoiding foods with cholesterol. He says it is undesirable to eat only vegetables and be on diets to lose weight.

Peiran Qiu

Peiran Qiu (1913-201097 years olda tenured professor of Shanghai University of Chinese Medicine. He is a famous educator and doctor of TCM.

One of Master Qius favorite students explaines his secret of longevity as following:

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"Tulasi" redirects here. For other uses, see Thulasi.

Ocimum tenuiflorum, also known as Ocimum sanctum, holy basil, or tulasi or tulsi (also sometimes spelled thulasi), is an aromatic plant in the family Lamiaceae which is native to the Indian subcontinent and widespread as a cultivated plant throughout the Southeast Asian tropics.[2][3] It is an erect, many-branched subshrub, 3060cm (1224in) tall with hairy stems and simple phyllotaxic green or purple leaves that are strongly scented.

Leaves have petioles and are ovate, up to 5cm (2.0in) long, usually slightly toothed. The flowers are purplish in elongate racemes in close whorls.[3] The two main morphotypes cultivated in India and Nepal are green-leaved (Sri or Lakshmi tulasi) and purple-leaved (Krishna tulasi).[4]

Tulasi is cultivated for religious and medicinal purposes, and for its essential oil. It is widely known across the Indian subcontinent as a medicinal plant and a herbal tea, commonly used in Ayurveda, and has an important role within the Vaishnava tradition of Hinduism, in which devotees perform worship involving holy basil plants or leaves. This plant is revered as an elixir of life.

The variety of Ocimum tenuiflorum used in Thai cuisine is referred to as Thai holy basil (Thai: kaphrao);[2] it is not to be confused with Thai basil, which is a variety of Ocimum basilicum.

DNA barcodes of various biogeographical isolates of Tulsi from the Indian subcontinent are now available. In a large-scale phylogeographical study of this species conducted using chloroplast genome sequences, a group of researchers from Central University of Punjab, Bathinda, have found that this plant originates from North Central India.[5][6] The discovery might suggest the evolution of Tulsi is related with the cultural migratory patterns in the Indian subcontinent.

Tulsi leaves are an essential part in the worship of Vishnu and his avatars, including Krishna and Ram, and other male Vaishnava deities such as Hanuman, Balarama, Garuda and many others. Tulsi is a sacred plant for Hindus and is worshipped as the avatar of Lakshmi.[7] It is believed that water mixed with the petals given to the dying raises their departing souls to heaven.[8]Tulsi, which is Sanskrit for "the incomparable one", is most often regarded as a consort of Krishna in the form of Lakshmi.[9][10] According to the Brahma Vaivarta Purana, tulsi is an expression of Sita.[11][full citation needed] There are two types of tulsi worshipped in Hinduism: "Rama tulsi" has light green leaves and is larger in size; "Shyama tulsi" has dark green leaves and is important for the worship of Hanuman.[12] Many Hindus have tulasi plants growing in front of or near their home, often in special pots. Traditionally, tulsi is planted in the centre of the central courtyard of Hindu houses. It is also frequently grown next to Hanuman temples, especially in Varanasi.[13][full citation needed]

According to Vaishnavas, it is believed in Puranas that during Samudra Manthana, when the gods win the ocean-churning against the asuras, Dhanvantari comes up from the ocean with Amrit in hand for the gods. Dhanvantari, the divine healer, sheds happy tears, and when the first drop falls in the Amrit, it forms tulasi. In the ceremony of Tulsi Vivaha, tulsi is ceremonially married to Krishna annually on the eleventh day of the waxing moon or twelfth of the month of Kartik in the lunar calendar. This day also marks the end of the four-month Chaturmas, which is considered inauspicious for weddings and other rituals, so the day inaugurates the annual marriage season in India. The ritual lighting of lamps each evening during Kartik includes the worship of the tulsi plant, which is held to be auspicious for the home. Vaishnavas especially follow the daily worship of tulsi during Kartik.[14] In another legend, Tulsi was a pious woman who sought a boon to marry Vishnu. Lakshmi, Vishnu's consort, cursed her to become a plant in earth. However, Vishnu appeased her by giving her a boon that she would grace him when he appears in the form of Shaligrama in temples.[15]

Vaishnavas traditionally use Hindu prayer beads made from tulsi stems or roots, which are an important symbol of initiation. Tulsi rosaries are considered to be auspicious for the wearer, and believed to put them under the protection of Hanuman. They have such a strong association with Vaishnavas, that followers of Hanuman are known as "those who bear the tulsi round the neck".[10]

Tulsi grown in front of a house

An altar with tulsi plant for daily worship in a courtyard in India

Tulasi (Sanskrit:-Surasa) has been used for thousands of years in Ayurveda for its diverse healing properties. It is mentioned in the Charaka Samhita,[16] an ancient Ayurvedic text. Tulsi is considered to be an adaptogen,[17] balancing different processes in the body, and helpful for adapting to stress.[18] Marked by its strong aroma and astringent taste, it is regarded in Ayurveda as a kind of "elixir of life" and believed to promote longevity.[19]

Tulasi extracts are used in ayurvedic remedies for a variety of ailments. Traditionally, tulasi is taken in many forms: as herbal tea, dried powder, fresh leaf or mixed with ghee. Essential oil extracted from Karpoora tulasi is mostly used for medicinal purposes and in herbal cosmetics.

The leaves of holy basil, known as kaphrao in the Thai language (Thai: ), are commonly used in Thai cuisine.[20]Kaphrao should not be confused with horapha (Thai: ), which is normally known as Thai basil,[20] or with Thai lemon basil (maenglak; Thai: ).

The best-known dish made with this herb is phat kaphrao (Thai: ) a stir-fry of Thai holy basil with meats, seafood or, as in khao phat kraphao, with rice.[21][22][23]

For centuries, the dried leaves have been mixed with stored grains to repel insects.[24] In Sri Lanka this plant is used as a mosquito repellent. Sinhala: Maduruthalaa

Some of the main chemical constituents of tulsi are: oleanolic acid, ursolic acid, rosmarinic acid,[25]eugenol, carvacrol, linalool, -caryophyllene (about 8%),[17]-elemene (c.11.0%), and germacrene D (about 2%).[26]

Isolated O. sanctum extracts have some antibacterial activity against E. coli, S. aureus and P. aeruginosa.[27]

The genome of Tulsi plant has been sequenced and the draft genome has been published independently by research teams from CSIR-Central Institute of Medicinal and Aromatic Plants at Lucknow and National Centre for Biological Sciences at Bengaluru. The genome size was estimated to be 612 mega bases and results from the sequencing project show that certain metabolite-biosynthesis genes such as genes for biosynthesis of Anthocyanin in Krishna Tulsi variety, Ursolic acid and Eugenol in Rama Tulsi variety were expressed in large quantities. These metabolites were shown to have anti-cancerous properties as well. It was further commented that these metabolites could be utilized as anti-cancerous drugs.[28]

Pattanayak, Priyabrata; Behera, Pritishova; Das, Debajyoti; Panda, Sangram (Jul 10, 2010). "Ocimum sanctum Linn. A reservoir plant for therapeutic applications: An overview". Pharmacognosy Reviews. 4 (7): 95105. doi:10.4103/0973-7847.65323. PMC3249909. PMID22228948.

Media related to Ocimum tenuiflorum at Wikimedia Commons

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Bio identical hormone balancing for men and women in menopause and andropause; Hormone replacement with bio identical hormone pellets,creams and injections. Intravenous vitamin infusions, New technique for High Dose Hyperbaric Ozone therapy,Prolozone, All modalities of Ozone administration Detoxification including intravenous chelation therapy. Functional and Alternative Medicine

Established in 2005.

Dr Liebowitz is a three times Board Certified Emergency Medicine Physician who practiced at Cedars Sinai Hospital in Los Angeles for over 15 years. He experienced many of his patients not getting better and returning to the ER with so many complications from the medications they were taking, that he felt there must be a better way to heal. He studied Functional Medicine and Anti Aging Medicine and realized that people could become healthier when all the normal functions of the body are supported. He integrates multiple disciplines of medicine from 30 years of experience together into his own unique blend. By balancing hormones, supporting the immune system,detoxification along with optimal diet and exercise (His 5 Step REDDI Plan)the result is optimal health with minimal or no pharmaceutical medications.

Dr. Liebowitz was trained in Internal Medicine at USC, and worked as an Emergency and Trauma Physician for 15 years at Cedars Sinai Medical Center in Los Angeles. He served as the Medical Director at The Centinela Hospital Fitness Institute in Los Angeles, testing professional athletes from The Lakers, Clippers, Dodgers and PGA golf tour. He also served as the team Doctor for The Pioneer Triathlon Team, a professional triathlon team. As a member of the medical steering committee for Tri-Fed, the governing body of the Triathlon sport, he helped direct it into the Olympics. He was a member of the advisory board of Bally Health and Tennis and 24 Hour Fitness, as well as a Physician at the Pritikin Longevity Center in Santa Monica, California. He has been a lifelong athlete himself as a college swimmer and later a triathlete completing the grueling Hawaii Ironman three times. His pursuit of helping athletes perform to their maximum potential naturally led him t

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Liebowitz Longevity Medicine - Santa Monica - yelp.com

At Longevity Medicalwe have assembled one of the finest groups of integrative physicians in the country. Many of our physicians are considered by their peers to be leaders in their field. In addition to providing excellent patient care, our physicians author research papers, lecture at medical conferences, as well as hold free medical lectures for our patients.

We recognize the importance of having a fully supportive environment, and that includes a caring staff. From your first phone call we are here to aid each patient through the process of scheduling, insurance, retrieving records, explaining treatment plans, and most of all getting you onto the path of health.

Meet our Staff picture from above, pictured Left to Right:

Leticia (Lead Medical Assistant), Tracy (Front Office Medical Assistant), Karina (Front Office Medical Assistant), Tami (Patient Care Coordinator)

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Physicians & Staff |Longevity Medical

Some people are more predisposed to suffer Parkinson's disease than others, a fraction of those due to mutations in genes involved in mitochondrial quality control. The state of mitochondrial function shows up as an important component of many different conditions and indeed in aging itself. In Parkinson's disease it is thought that mitochondrial dysfunction contributes to the conditions in which the population of dopamine-producing neurons in the brain die off, producing the characteristic symptoms of the disease.

It may be that more of Parkinson's disease is genetic than was previously thought, and the odds of that being the case increase as the chain of molecular machinery involved in mitochondrial quality control is followed and new components identified. This sort of work also helps clarify the mechanisms associated with mitochondrial dysfunction in aging:

Mitofusin 2 (Mfn2) is known for its role in fusing mitochondria together, so they might exchange mitochondrial DNA in a primitive form of sexual reproduction. "Mitofusins look like little Velcro loops. They help fuse together the outer membranes of mitochondria. Mitofusins 1 and 2 do pretty much the same thing in terms of mitochondrial fusion. What we have done is describe an entirely new function for Mfn2."

Mitochondria work to import a molecule called PINK. Then they work to destroy it. When mitochondria get sick, they can't destroy PINK and its levels begin to rise. Once PINK levels get high enough, they make a chemical change to Mfn2, which sits on the surface of mitochondria. This chemical change is called phosphorylation. Phosphorylated Mfn2 on the surface of the mitochondria can then bind with a molecule called Parkin that floats around in the surrounding cell.

Once Parkin binds to Mfn2 on sick mitochondria, Parkin labels the mitochondria for destruction. The labels then attract special compartments in the cell that "eat" and destroy the sick mitochondria. As long as all links in the quality-control system work properly, the cells' damaged power plants are removed, clearing the way for healthy ones. "But if you have a mutation in PINK, you get Parkinson's disease. And if you have a mutation in Parkin, you get Parkinson's disease. About 10 percent of Parkinson's disease is attributed to these or other mutations that have been identified." The discovery of Mfn2's relationship to PINK and Parkin opens the doors to a new genetic form of Parkinson's disease.

Link: http://www.sciencedaily.com/releases/2013/04/130425142357.htm

Source:
http://www.fightaging.org/archives/2013/04/joining-the-dots-in-genetic-parkinsons-disease.php

A conservative view of what lies ahead for Alzheimer's disease (AD) research sees incremental progress resulting from new and better investigative biotechnologies:

In the recently published work "The Biology of Alzheimer Disease" (2012), most of what is known about AD today is described in detail. The book culminates in a chapter called Alzheimer Disease in 2020, where the editors extol "the remarkable advances in unraveling the biological underpinnings of Alzheimer disease...during the last 25 years," and yet also recognize that "we have made only the smallest of dents in the development of truly disease modifying treatments." So what can we reasonably expect over the course of the next 7 years or so? Will we bang our heads against the wall of discovery, or will there be enormous breakthroughs in identification and treatment of AD?

Though a definitive diagnosis of AD is only possible upon postmortem histopathological examination of the brain, a thorough review of the book leads me to believe that the greatest progress currently being made is in developing assays to diagnose AD at earlier stages. It is now known that neuropathological changes associated with AD may begin decades before symptoms manifest. This, coupled with the uncertainty inherent in a clinical diagnosis of AD, has driven a search for diagnostic markers. Two particular approaches have shown the most promise: brain imaging and the identification of fluid biomarkers of AD.

The authors anticipate that advances in whole-genome and exome sequencing will lead to a better understanding of all of the genes that contribute to overall genetic risk of AD. Additionally, improved ability to sense and detect the proteins that aggregate in AD and to distinguish these different assembly forms and to correlate the various conformations with cellular, synaptic, and brain network dysfunction should be forthcoming in the next few years. Lastly, we will continue to improve our understanding of the cell biology of neurodegeneration as well as cell-cell interactions and inflammation, providing new insights into what is important and what is not in AD pathogenesis and how it differs across individuals, which will lead, in turn, to improved clinical trials and treatment strategies.

Link: http://www.alcor.org/magazine/2013/08/21/alzheimer-disease-in-2020/

Source:
https://www.fightaging.org/archives/2013/08/the-next-few-years-of-research-into-alzheimers-disease.php

What is aging? This deceptively simple question will garner you lengthy answers from the scientific community - many different lengthy answers, as it happens, some of which are even long enough to take the form of entire, complete books. There is a lot to be said on aging, and vast repositories of data, and yet there remain numerous different camps with different detailed definitions of aging - it's cause, its progression, and how best to build therapies that might slow or reverse aging.

So you have the definition put forward by Michael Rose and colleagues, or the hyperfunction theories that seem to be gaining ground among researchers of the small programmed aging camp, or the collection of mainstream views - many different interpretations and variants - that paint aging as a matter of accumulated damage.

And that is just on the matter of causes and mechanisms. The territory becomes much more of a jungle once you start down the path of asking whether aging is a disease, or whether it is a bad thing, or whether should be treated and ameliorated through medical science. Believe it or not there remain numerous researchers in the field who believe that aging should be studied but not treated, slowed, or reversed, despite the suffering and death it causes. Here is an open access opinion piece on this topic from Aubrey de Grey, via the Rejuvenation Research journal.

The desperate need for a biomedically useful definition of "aging" (PDF)

Surely everyone who studies the biology of aging fundamentally agrees on what it is they are studying, even if they may prefer somewhat different terminology to define it? I'm afraid you'd be wrong. Disagreement within the field about what aging really is and is not is very far from purely semantic, and the substance of those disagreements leads to profound differences of opinions concerning both what research gerontologists should prioritise and how they should communicate their work to others.

First: is aging a disease? Some gerontologists will just tell you "No, it is separate from age-related diseases". Some will say "No, but it is a risk factor for age-related diseases". Some will say "No, it is the set of precursors of the age-related diseases". Some will say "Yes, it is the set of precursors of the age-related diseases"! Self-evidently, whether X is a Y depends not only on the definition of X but also on the definition of Y, so one might excuse this chaos on the basis of a failure to agree on what is and is not a disease - and there is indeed no such agreement. But it gets worse.

Is aging a thing that is amenable, in principle, to medical intervention? Not if you believe the protestations of such eminent gerontologists as Bruce Carnes and Jay Olshansky, who in a recent paper critiquing (I employ classic British understatement in my choice of words here) various colleagues' work made, in spite of reviewers' efforts to educate them, the assertion that "What Wilmoth fails to acknowledge is that in order to reduce death rates at advanced ages to zero or close to it, our biology would need to be modified" (my emphasis). This sort of language, without stating explicitly that medicine can never maintain the body in a state of health so youthful that death rates will be vastly lower than today, unequivocally seeks to convey that view. So, do other gerontologists agree? Indeed they do not: if any evidence were needed, I may merely cite the fact that almost every mainstream conference on the biology of aging these days has a subtitle referring to delaying or even reversing aging.

Finally, is aging even a bad thing? At least here we find broad consensus among biogerontologists - those who study the biology of aging (though there are a few exceptions). But the same does not apply to all gerontologists: those whose field is more on the clinical, or the sociological, side tend to be among the most viciously and vocally opposed to any talk (let alone action) concerning actually doing anything about aging. As an example, a very senior (and, I am afraid to say, highly influential) clinical gerontologist from Canada recently wrote to me as follows: "I do not wish in any way shape or form to have my name associated with anti-aging medicine, regenerative or restorative medicine or some such". No kidding. I will be interested to discover, at some point, whether she is willing to defend that view publicly.

It should by now be apparent that there is a bit of a problem. Let me emphasise, however, just how much of a problem. At present, translational biogerontology (alternatively, biomedical gerontology) commands an absolutely minuscule proportion of the medical research budget of any industrialised nation. Why? Simply because the idea that postponing aging is a feasible and valuable goal, both socially and economically, has failed - despite the best efforts of many biogerontologists over many decades - to gain any significant traction among funding bodies.

I contend that gerontologists' muddled thinking outlined above concerning what aging really is is actually the number one reason for this failure.

Source:
http://www.fightaging.org/archives/2013/03/in-search-of-a-useful-scientific-definition-for-aging.php

Without the biotechnologies of human rejuvenation that could be created over the next twenty years given a fully funded crash program of development, we and our descendants will all die due to the effects of aging, exactly as did our ancestors. Aging to death has never been a choice - but now it is, and every needless day of delay comes at a cost of 100,000 lives. Everyone presently alive will suffer greatly due to aging and age-related conditions unless new medical technologies of the sort envisaged by the SENS Research Foundation are developed to repair and reverse the low-level biological damage that causes of aging. So why isn't this front and center on everyone's list of concerns? Why does longevity science and the elimination of age-related suffering barely even register in public eye?

Here is a talk on this subject given at the Stanford Advancing Humanity Symposium last month by Maria Konovalenko of the Russian Science For Life Extension Foundation, an advocacy initiative:

In this talk I am sharing our wonder about why haven't the ideas of life extension won. It is not clear why isn't every person on Earth concerned with their longevity. There are several serious reasons that I mention in my presentation, but even all of them combined don't give the answer to this question. I am also looking at different possible scenarios of how the extending longevity ideas could rise to power.

Source:
http://www.fightaging.org/archives/2013/04/why-isnt-longevity-science-the-worlds-greatest-concern.php

Philanthropy by high net worth individuals has the potential to move the needle on any major biotechnology project these days. The cost of research in the field is falling rapidly, thanks to spectacular ongoing gains in computational power and materials science. There are now thousands of individuals in the world with a net worth sufficient to completely fund a cure for a disease, from a starting point of nothing but ideas through to first human trials. But of course to exchange your entire net worth for a cure, to give up on the whole of the vast process that has been your business life to date, you'd have to be something of a visionary zealot - and people tend not to be both very wealthy and visionary zealots of this nature; the two paths are mutually exclusive.

The cost to develop the various biotechnologies of rejuvenation enumerated in the SENS vision - a digest of discoveries from the past twenty years in many fields of the life sciences, coupled with innovative, detailed plans to develop therapies - might be in the vicinity of a billion dollars over ten to twenty years. That would give you a good chance at demonstrating rejuvenation in old mice, such as by doubling their remaining life span, with commensurate improvements in their health and reductions in risk of age-related disease. There are perhaps a hundred people in the world who could fund that project end to end on 10% of their net worth or less, though as I've noted in the past a billionaire is possibly best viewed more as the head of a city-state than a person with complete agency over their own fortune.

One portion of the advocacy and fundraising for new approaches to longevity science like SENS involves gathering a strong grassroots community and leaning on their modest financial support. This sort of activity typically takes place during the bootstrapping phase of development, and in the process validates your cause in the eyes of established funding sources, high net worth philanthropists, and so forth. These institutions and individuals tend to be very conservative in how they devote their resources to scientific projects, which means that you must have some backing and widespread validation in order to become an attractive recipient. So it has traditionally been the case that you can't really make too much of a mark without both a broad base of support among the public and interested followers, and then atop that some circle of people and institutions capable of devoting large-scale funding to solving specific problems. The rise of crowdfunding is changing that balance, but it still generally holds - it's the rare organization that manages to skip past the need for wealthy donors due to the size and strength of its community.

Given all of this you might look at the advocacy and outreach for SENS or other disruptive, next-generation, high-yield approaches to extending healthy human life as something that has three components:

• Convince the scientific community.
• Convince the general public.
• Convince high net worth donors and funding institutions.

In the third category, there is the constant process of networking - connections, discussions, and introductions that we don't see all that much of from the outside - but there is also the matter of messaging via channels aimed at the wealthier and more influential portions of society. One example of that is a recent article by researcher and advocate Aubrey de Grey in the Private Journey, a magazine aimed at luxury consumers. Via the Reddit SENS community, I note that a PDF copy can be downloaded from the SENS Research Foundation site archives:

The Undoing of Aging

The desire to defeat aging is surely even more long-standing than the quest to reach the stars. Unfortunately, the idea that we will crumble and die is so crippling that most people evidently need to convince themselves, by whatever means, that it is not such a bad thing after all. Whether it's the existence of a joyous afterlife, or the presumption that a post-aging world would be unsustainably overpopulated, or the fear of immortal dictators, a conversation with nearly anyone about the idea of developing medicine to prevent age-related ill-health is almost certain to be derailed into arguments about whether such medicine would be a good thing at all.

A key pillar of many people's thinking about this topic is the misconception that "aging itself" is somehow a different sort of thing than the diseases of old age. There is actually no such distinction. Age-related diseases spare young adults simply because they take a long time to develop, and they affect everyone who lives long enough because they are side-effects of the body's normal operation rather than being caused by external factors such as infections. In other words, aging is simply the collection of early stages of the diseases and disabilities of old age, and treatment of aging is simply preventative medicine for those conditions - preventative geriatrics. It is thus logically incoherent to support medicine for the elderly but not medicine for aging.

I claim no originality for the above: it has long been the virtually universal view of those who study the biology of aging. I believe it is resisted by the wider world, despite those experts' energetic efforts, overwhelmingly because people don't believe there is much chance of significant progress in their or even their children's lifetimes and they don't want to get their hopes up. But in recent years, the justification for such pessimism has evaporated.

It has done so above all because of progress in regenerative medicine, which colloquially (but see below) consists of stem cells and tissue engineering. Regenerative medicine can be defined as the restoration of bodily function by restoration of structure. We may replace entire organs (tissue engineering), or we may repair organs by replacing their constituent cells (stem cell therapy). In a sense, regenerative medicine is maintenance for the human body. as such, it should in principle be capable of constituting preventative maintenance for the chronic, slowly progressive, initially harmless but eventually fatal processes that jointly make up aging and the diseases of old age. Regenerative medicine has only recently, however, become recognized as a promising avenue for postponing age-related ill-health. This is for two reasons. firstly, it was originally conceived and pursued for its potential to treat acute injury, such as spinal cord trauma, rather than chronic damage: thus, regenerative medicine pioneers and biologists of aging simply didn't talk to each other very much, with the result that those studying aging were insufficiently informed about progress in regenerative medicine to appreciate its potential. The second reason was equally important: in order to be plausibly applicable to aging, regenerative medicine must be broadened into a host of other areas, over and above stem cells and tissue engineering, and those areas are mostly at considerably earlier stages of development.

But not fancifully early. In the decade since I first laid out a putatively comprehensive classification of the various types of molecular and cellular "damage" that must be periodically repaired in order to stave off the decline of old age, and the specifics of how we might do it, progress has been gratifyingly rapid (though I estimate it could be at least three times faster if the potential of this approach were more widely understood and funding for it correspondingly elevated). Furthermore, that plan has abundantly stood the test of time, undergoing only minor adjustments.

In this short, general-audience piece I can only hint at the advances over the past year or two achieved by researchers worldwide in this space. SENS Research Foundation was created for this purpose, and alongside numerous other institutes and organizations, both commercial and nonprofit, we have achieved not only the retardation of aging but its actual repair, restoring youthful health to animals that were suffering widespread age-related decline. Much remains to be done to extend these results, before they can realistically be applied in the clinic. However, the removal of toxic metabolic by-products shows clear promise of completely eliminating cardiovascular disease, the Western world's foremost killer, and also macular degeneration, the leading cause of blindness in the elderly. Similarly, removing cells that have become dysregulated and toxic to the body was recently shown, in multiple models, to restore function to sick animals. Advances like these, in combination with traditional regenerative medicine, may in the next few decades deliver a truly comprehensive and dramatic postponement of age-related ill-health.

Source:
http://www.fightaging.org/archives/2013/04/aubrey-de-grey-on-the-undoing-of-aging.php

Calorie restriction slows the progression of near all measurable aspects of degenerative aging, and improves near all measures of health. It extends life by up to 40% in mice, and one of the interesting challenges for the study of metabolism is to explain the mechanics of how it can improve health so greatly in humans while failing to extend life to the same degree as it does in shorter-lived mammals. There is a good evolutionary explanation for this phenomenon; the expected length of a naturally occurring famine is the same whether you are a mouse or a man, and thus life span changes in response to famine must be more dramatic in a shorter lived species in order to have a decent chance of surviving it to reproduce. But that doesn't tell us how it happens under the hood.

Some of the triggers for the metabolic changes of calorie restriction involve sensing protein levels. Maintaining the same calorie intake while reducing dietary protein levels captures some fraction of the full effects of calorie restriction, with methionine seemingly the most important triggering protein.

Here a noted calorie restriction researcher shows protein restriction to slow the progression of a mouse model of Alzheimer's disease - which is pretty much the expected result, given what we know so far of how the effects of protein restriction map to those of calorie restriction:

Low-protein diet slows Alzheimer's in mice

Mice with many of the pathologies of Alzheimer's Disease showed fewer signs of the disease when given a protein-restricted diet supplemented with specific amino acids every other week for four months. Mice at advanced stages of the disease were put on the new diet. They showed improved cognitive abilities over their non-dieting peers when their memory was tested using mazes. In addition, fewer of their neurons contained abnormal levels of a damaged protein, called "tau," which accumulates in the brains of Alzheimer's patients.

Upcoming studies [will] attempt to determine whether humans respond similarly - while simultaneously examining the effects of dietary restrictions on cancer, diabetes and cardiac disease. "We had previously shown that humans deficient in Growth Hormone receptor and IGF-I displayed reduced incidence of cancer and diabetes. Although the new study is in mice, it raises the possibility that low protein intake and low IGF-I may also protect from age-dependent neurodegeneration."

The team found that a protein-restricted diet reduced levels of IGF-1 circulating through the body by 30 to 70 percent, and caused an eight-fold increase in a protein that blocks IGF-1's effects by binding to it. IGF-1 helps the body grow during youth but is also associated with several diseases later in life in both mice and humans. Exploring dietary solutions to those diseases as opposed to generating pharmaceuticals to manipulate IGF-1 directly allows Longo's team to make strides that could help sufferers today or in the next few years.

"We always try to do things for people who have the problem now. Developing a drug can take 15 years of trials and a billion dollars. Although only clinical trials can determine whether the protein-restricted diet is effective and safe in humans with cognitive impairment, a doctor could read this study today and, if his or her patient did not have any other viable options, could consider introducing the protein restriction cycles in the treatment - understanding that effective interventions in mice may not translate into effective human therapies."

You might take note of those last remarks as indicative of one of the ways in which regulation steers researchers towards deliberately aiming to produce marginal benefits rather than revolutionary advances - slowing the pace of progress and shutting down promising avenues of medical science before they even get started.

Source:
http://www.fightaging.org/archives/2013/02/protein-restriction-slows-progression-of-mouse-model-of-alzheimers-disease.php

One of the root causes of aging is the formation of advanced glycation end-products (AGEs), something that happens much faster in a diabetic metabolism, but which nonetheless happens to all of us and causes progressively greater harm as the years pass. AGEs gum together and disable vital protein machinery, and also hammer on cell receptors in ways that cause chronic inflammation and other ills.

Past work on ways to break down AGEs - AGE-breaker drugs - largely occurred prior to the present rapid pace of development in biotechnology, and was both laborious and ultimately of little use in people despite promising animal studies. It turned out that the most important types of AGE in long-lived humans are not the same as in short-lived rodents, and thus drugs that help rats do little for people. However, one single form of human AGE - glucosepane - does make up the vast, overwhelming majority of AGEs in tissues such as skin. So it is a very viable, narrow target now that the research community knows enough to identify it as the primary target.

A safe way to remove glucosepane is needed in order to largely eliminate this contribution to degenerative aging. Sadly, as for much of the foundations of future rejuvenation therapies, little work and funding is directed to this end. This is thus one of the areas in which the SENS Research Foundation hopes to step in and spur greater interest and progress. Here are some notes on the current research programs funded by the Foundation to this end:

Chemical "crosslinking" of the structural proteins of our arteries slowly stiffens them with age, leading to more rigid blood vessels, rising "systolic" blood pressure (the first or top number in a blood pressure reading), and eventually to the loss of the ability of the kidneys to filter toxins from our blood, and a rising risk of stroke with age. Rejuvenation biotechnology can prevent these scourges at their source. New medicines that break apart these molecular "handcuffs" would allow the proteins of the arteries could move freely again, restoring the supple flexibility and cushioning capacity of aging arteries to youthful health and functionality. As a result, damage to the kidneys would be prevented, and strokes averted.

With a generous donation from software entrepreneur Jason Hope, SENS Research Foundation and the Cambridge University Institute of Biotechnology have established a new SENS Research Foundation Laboratory at Cambridge. With no one else taking on this challenging, critical research, the scientists in the Cambridge SENS lab will initiate work on biomedical solutions to glucosepane crosslinks starting from the ground up - with research to develop reagents that can rapidly and specifically detect proteins that have been crosslinked by glucosepane. The development of such reagents is an indispensible enabling technology for the development and testing of candidate glucosepane-breaking drugs.

In parallel, SENS Research Foundation is also providing funding to Dr. David Spiegel's group at Yale University, which has special expertise in making glycation crosslinks and which has recently been studying the mechanisms and chemical vulnerabilities of precursors of glucosepane. Dr. Spiegel's group has also recently published a report clarifying how the first generation crosslink-breaking drug worked. Once the Cambridge SRF lab has successfully established methods for identifying proteins that have been handcuffed together by glucosepane, Dr. Spiegel's group will use them to begin developing potential glucosepane-cleaving agents. Completing the cycle, candidate agents can then be tested at the Cambridge center - initially in tissue culture, and eventually in vivo.

Once developed, any glucosepane-labeling reagents that emerge from the first phase of this work will made available as openly as possible, to accelerate research into the role of crosslinks in disease and aging, and into ways to combat them.

Link: http://www.sens.org/research/research-blog/project-break-aging-arteries-free

Source:
http://www.fightaging.org/archives/2013/03/sens-research-foundations-age-breaker-research-programs.php

Alpha-synuclein is associated with Parkinson's disease (PD), and is believed to play a central role in the mechanisms that cause the destruction of dopamine-generating neurons, and thus the pathology of the condition. Here, researchers dig deeper into the processes involved:

Overexpression of a protein called alpha-synuclein appears to disrupt vital recycling processes in neurons, starting with the terminal extensions of neurons and working its way back to the cells' center, with the potential consequence of progressive degeneration and eventual cell death. "This is an important new insight. I don't think anybody realized just how big a role alpha-synuclein played in managing the retrieval of worn-out proteins from synapses and the role of alterations in this process in development of PD."

Using a variety of leading-edge imaging technologies, including a new fluorescent tagging technique developed for electron microscopy, [the] scientists created three-dimensional maps of alpha-synuclein distribution both in cultured neurons and in the neurons of mice engineered to over-express the human protein. They found that excess levels of alpha-synuclein accumulated in the presynaptic terminal - part of the junction where axons and dendrites of brain cells meet to exchange chemical signals.

"The over-expression of alpha-synuclein caused hypertrophy in these terminals. The terminals were enlarged, filled with structures we normally don't see." [As] alpha-synuclein accumulates in the terminals, it appears to hinder normal degradation and recycling processes in neurons. This would progressively impair the release of neurotransmitters. In time, the neurons might simply stop functioning and die.

Link: http://www.sciencedaily.com/releases/2013/02/130207141402.htm

Source:
http://www.fightaging.org/archives/2013/02/parkinsons-disease-as-localized-garbage-catastrophe.php

A new candidate for building an Alzheimer's therapy shows promise in mice:

When a molecule called TFP5 is injected into mice with disease that is the equivalent of human Alzheimer's, symptoms are reversed and memory is restored - without obvious toxic side effects. "We hope that clinical trial studies in AD patients should yield an extended and a better quality of life as observed in mice upon TFP5 treatment. Therefore, we suggest that TFP5 should be an effective therapeutic compound."

To make this discovery, [researchers] used mice with a disease considered the equivalent of Alzheimer's. One set of these mice were injected with the small molecule TFP5, while the other was injected with saline as placebo. The mice, after a series of intraperitoneal injections of TFP5, displayed a substantial reduction in the various disease symptoms along with restoration of memory loss. In addition, the mice receiving TFP5 injections experienced no weight loss, neurological stress (anxiety) or signs of toxicity. The disease in the placebo mice, however, progressed normally as expected. TFP5 was derived from the regulator of a key brain enzyme, called Cdk5. The over activation of Cdk5 is implicated in the formation of plaques and tangles, the major hallmark of Alzheimer's disease.

Link: http://www.eurekalert.org/pub_releases/2013-01/foas-pcr010213.php

Source:
http://www.fightaging.org/archives/2013/01/tfp5-shows-promise-for-treating-alzheimers-disease.php

Over at In Search of Enlightenment you'll find an unpublished interview where the questions somewhat illustrate the point that most people don't look much beyond trivial matters when it comes to aging and longevity. Biotechnology like SENS and similar research projects are given no thought at all in most quarters, and even amongst advocates many favor the snail's pace path of trying to slow aging rather than working to repair its root causes to reverse it. This all means that there is much yet to accomplish in advocacy and education.

The field of research known as biogerontology, which studies the biology of aging, is a truly fascinating, though often misunderstood, area of scientific research. In 2011 the genome of the naked-mole rat was sequenced. This rodent is only the size of a mouse, and one might wonder what the significance of sequencing its genome could possibly be. But the naked-mole rate is the longest living rodent, it has a maximum lifespan exceeding 30 years and an exceptional resistance to cancer. Understanding the biology of this species could help unlock the mystery of healthy aging. A variety of experiments on fruit flies, mice and other species have demonstrated that the rate of aging can be manipulated, either by calorie restriction or by activating particular genes. Such research could eventually lead to the development of a drug that safely mimics the effects of caloric restriction (which delays the onset of disease) or actives the "longevity genes" that help protect against the diseases of late life.

The lion's share of funding for medical research is spent on disease research, such as research on cancer, heart disease or Alzheimer's disease. This approach, which I call "negative biology", assumes that the most important question to answer is "what causes disease?". Unfortunately this is a severely limited approach, especially for older populations. Even if you cured all 200+ forms of cancer (and we have not yet eliminated even just one cancer despite investing enormous sums of money for decades now), one of the other diseases of aging would quickly replace cancer as the leading cause of death because most people in late life are vulnerable to multiple diseases. So "positive biology" takes a different intellectual starting point. It assumes that the puzzles of exemplar health are just as important to understand as the development of disease. How can some (very rare) humans live over a century of disease-free life? Understanding these exemplar examples of health might prove to be more significant than trying to understand, treat and cure every specific disease of late life.

Link: http://colinfarrelly.blogspot.com/2012/12/readers-digest-interview-on-aging-and.html

Source:
http://www.fightaging.org/archives/2013/01/unpublished-readers-digest-interview-on-aging-and-longevity.php

The most visible signs of Parkinson's disease are caused by the progressive destruction of a comparatively small population of dopamine-generating neurons in the brain. But why these cells? A full answer to that question might lead to ways to block progression of the condition:

Neuroinflammation and its mediators have recently been proposed to contribute to neuronal loss in Parkinson's, but how these factors could preferentially damage dopaminergic neurons has remained unclear until now. [Researchers] were looking for biological pathways that could connect the immune system's inflammatory response to the damage seen in dopaminergic neurons. After searching human genomics databases, the team's attention was caught by a gene encoding a protein known as interleukin-13 receptor alpha 1 chain (IL-13Ra1), as it is located in the PARK12 locus, which has been linked to Parkinson's.

IL-13r?1 is a receptor chain mediating the action of interleukin 13 (IL-13) and interleukin 4 (IL-4), two cytokines investigated for their role as mediators of allergic reactions and for their anti-inflammatory action. With further study, the researchers made the startling discovery that in the mouse brain, IL-13Ra1 is found only on the surface of dopaminergic neurons. "This was a 'Wow!' moment."

The scientists set up long-term experiments using a mouse model in which chronic peripheral inflammation causes both neuroinflammation and loss of dopaminergic neurons similar to that seen in Parkinson's disease. The team looked at mice having or lacking IL-13Ra1 and then compared the number of dopaminergic neurons in the brain region of interest. The researchers expected that knocking out the IL-13 receptor would increase inflammation and cause neuronal loss to get even worse. Instead, neurons got better.

If further research confirms the IL-13 receptor acts in a similar way in human dopaminergic neurons as in mice, the discovery could pave the way to addressing the underlying cause of Parkinson's disease. Researchers might, for instance, find that drugs that block IL-13 receptors are useful in preventing loss of dopaminergic cells during neuroinflammation.

Link: http://www.scripps.edu/news/press/2012/20121119conti.html

Source:
http://www.fightaging.org/archives/2012/11/towards-an-understanding-of-why-dopamine-neurons-are-vulnerable-in-parkinsons-disease.php

You might recall past studies of elite atheletes that showed a sizable correlation with increased life expectancy:

• Atheletes Live Longer, Probably the Exercise
• Putting Upper Bounds on Longevity Derived From Exercise

Exercise and physical fitness are obviously things to point to here. Causation is harder to pin down in human studies: for example, we might ask to what degree competitive athletes are drawn their line of work because they are more robust than the average individual - and thus capable of living longer anyway. While it's certainly the case that a mountain of studies show causation for health benefits deriving from moderate exercise, there isn't as much to point to when it comes to the same for human life expectancy. There is certainly a lot of correlation in published research, however.

There are any number of other significant factors at play here when you look at statistical differences of a few years up or down in human life expectancy. For example, wealth: successful professional athletes are wealthier than the average fellow. To what degree is their longer life expectancy the result of the broad array of benefits that come with being wealthier? Easier access to medicine; more personal connections where it matters; greater likelihood of education or other access to knowledge that helps with taking advantage of medicine; and so forth.

Here is another study that shows a longevity advantage for athletes, but which unfortunately doesn't help much with questions of causation:

Olympic medalists stay alive longer, study finds

Athletes who win at the Olympics may bring home more than just a medal: They could add a few years to their life spans, scientists have found. Winners of a gold (or silver or bronze) medal lived almost three years longer on average than their country's general population - when matched for age, gender and birth year - according to a study [that] examined some 15,174 Olympic medalists.

"Some elite sportspeople may be influenced by fame and glory, which could confer longevity through increased affluence," said an editorial accompanying the research, "unless undermined by excessive partying and hazardous risk-taking behaviors."

Alternatively, survival edges could simply be due to more healthful lifestyles and physical fitness. [Researchers] said it wasn't possible to examine the longevity fates of those who competed in the Olympics but did not win a medal because records for non-winners weren't nearly as complete as those for winners.

The study is open access and very readable, so head on over and have a look at the published paper. It isn't the first to suggest that high intensity regular exercise is either no more beneficial than moderate regular exercise or no more correlated with longevity:

Our results show that former Olympic athletes who engaged in disciplines with high cardiovascular intensity had similar mortality risks to athletes from disciplines with low cardiovascular intensity. This would indicate that engaging in cycling and rowing (high cardiovascular intensity) had no added survival benefit compared with playing golf or cricket (low cardiovascular intensity).

Source:
http://www.fightaging.org/archives/2012/12/life-expectancy-in-successful-atheletes-is-a-good-example-of-why-its-hard-to-pin-down-correlations-in-human-longevity.php

I noticed a good, comprehensible open access paper today: a review that summarizes what is known of the biology of the most common type of long-lived genetically engineered mouse species, those with disrupted or suppressed growth hormone (GH) activity. These include Ames dwarf mice, Snell dwarf mice, and growth hormone receptor knockout (GHRKO) mice. The present record for mouse longevity is held by the results of a GHRKO study, some of the mice involved living more than 60% longer than peers.

If you'd like to better understand how this all fits together under the hood and how it relates to other areas of study where metabolism, genetic engineering, and aging overlap - such as calorie restriction - then take a look:

Metabolic characteristics of long-lived mice

The remarkable extension of longevity in mice lacking GH or GH receptors appears to be due to multiple interacting mechanisms including reduced activation of growth-promoting pathways, greater stress resistance, reduced inflammation, increased reservoir of pluripotent stem cells, and improved genome maintenance.

Data summarized in this article indicate that alterations in energy metabolism and improved insulin control of carbohydrate homeostasis have to be added to this list. In fact, these metabolic adaptations may represent key features of the "longevous" phenotype of these animals and important mechanisms of the extension of both healthspan and lifespan in GH-related mutants.

Importantly, many of the metabolic features of long-lived mutant mice described in this article have been associated with extended human longevity. Comparisons between centenarians and elderly individuals from the same population and between the offspring of exceptionally long-lived people and their partners indicate that reduced insulin, improved insulin sensitivity, increased adiponectin, and reduced pro-inflammatory markers consistently correlate with improved life expectancy.

Source:
http://www.fightaging.org/archives/2012/12/an-introduction-to-whats-going-on-inside-long-lived-mice.php

Many dubious arguments are fielded in support of aging and involuntary death: every status quo, no matter how terrible, gathers its supporters. This is one of the deeper flaws inherent in human nature, the ability to mistake what is for the most desirable of what is possible. A hundred thousand deaths each and every day and the suffering of hundreds of millions is the proposal on the table whenever anyone suggests that human aging should continue as it is.

Massive campaigns of giving and social upheaval have been founded on the backs of a hundredth of this level of death and pain - but the world has a blindness when it comes to aging. Such is the power of the familiar and the long-standing: only heretics seek to overturn it, no matter how horrid and costly it is.

Nonetheless, this is an age of biotechnology in which aging might be conquered. There are plans and proposals, set forth in some detail, and debate over strategy in the comparatively small scientific community focused on aging research. So arguments over whether the development of means of rejuvenation should take place at all, reserved for philosophers and futurists in the past, now have concrete consequences: tens of millions of lives and untold suffering whenever progress is delayed. It should always be feared that a society will somehow turn to block or impede research into therapies for aging - worse and more outright crimes have been committed in the past by the members of so-called civilized cultures.

One of the arguments put forward in favor of a continuation of aging and mass death is that without the threat of impending personal extinction we'd collapse into stagnation and indolence. As the argument goes, only death and an explicitly limited future gives us the incentive to get anything done, and so all progress depends upon aging to death. I state the proposition crudely, but this is the essence of the thing, flowery language or no.

This is a terribly wrong way of looking at things: it denies the existence of desire independent of need. It casts us as nothing more than some form of Skinner box, unable to act on our own. This is another example of the way in which many humans find it hard to look beyond what is to see what might be: we live in a state of enforced urgency because we are all dying, because the decades of healthy life are a time of frantic preparation for the decline and sickness that comes later. It is normal, the everyday experience, for all of us to know we are chased by a ticking clock, forced to put aside the things that we would rather do in favor of the things that we must do. We cannot pause, cannot follow dreams, cannot stop to smell the roses.

Some people seem to manage these goals, but only the lucky few - and then only by twining what they would like to do with what they must do. It's hard to achieve that end, and it is really nothing more than an ugly compromise even when obtained. Yet like so much of what we are forced into by the human condition, it is celebrated. One more way in which what is triumphs over what might be in the minds of the masses.

Given many more healthy years of life in which to do so, we would lead quite different lives. Arguably better lives, not diverted by necessity into a long series of tasks we do not want to undertake, carried out for the sake of what will come. We could follow desire rather than need: work to achieve the aims that we want to achieve, not those forced on us. Because of aging and death, we are not free while we are alive - and in any collection of slaves there are those who fear the loss of their chains. The longer they are enslaved, the less their vision of freedom. Sadly, in the mainstream of our culture, it is those voices that speak the loudest.

Source:
http://www.fightaging.org/archives/2012/10/putting-aside-what-youd-rather-do-because-youre-dying.php

A range of age-related conditions are characterized by a buildup or clumping of harmful proteins, and research tends to focus first on ways to safely break down these compounds. Here researchers are testing a new candidate method of breaking down the beta amyloid and tau associated with Alzheimer's disease:

Last March, researchers at UCLA reported the development of a molecular compound called CLR01 that prevented toxic proteins associated with Parkinson's disease from binding together and killing the brain's neurons. Building on those findings, they have now turned their attention to Alzheimer's disease, which is thought to be caused by a similar toxic aggregation or clumping, but with different proteins, especially amyloid-beta and tau.

And what they've found is encouraging. Using the same compound, which they've dubbed a "molecular tweezer," in a living mouse model of Alzheimer's, the researchers demonstrated for the first time that the compound safely crossed the blood-brain barrier, cleared the existing amyloid-beta and tau aggregates, and also proved to be protective to the neurons' synapses - another target of the disease - which allow cells to communicate with one another.

Even though synapses in transgenic mice with Alzheimer's may shut down and the mice may lose their memory, upon treatment, they form new synapses and regain their learning and memory abilities. ... For humans, unfortunately, the situation is more problematic because the neurons gradually die in Alzheimer's disease. That's why we must start treating as early as possible. The good news is that the molecular tweezers appear to have a high safety margin, so they may be suitable for prophylactic treatment starting long before the onset of the disease.

Link: http://www.eurekalert.org/pub_releases/2012-11/uoc--rrp111512.php

Source:
http://www.fightaging.org/archives/2012/11/molecular-tweezers-versus-alzheimers-disease.php