Trehelose is known to be involved in yeast life span, and given in the diet can extend life in nematode worms. In animals closer to we humans, it has been show to stimulate autophagy, the collection of processes by which cells recycle damaged components and remove the unwanted build-up of metabolic byproducts. More autophagy seems to be an unqualified good, and shows up as a mechanism of action by which healthy life span is extended via calorie restriction (CR), exercise, and drugs that aim to mimic some of the biochemical changes caused by CR and exercise. This all makes sense: if damaged components are removed from cells more rapidly, they have less time to cause further damage themselves. The system as a whole is better maintained. So there is some impetus in the research community to develop the means to enhance autophagy in humans.

I noticed one small portion of that line of work today - an open access study in mice that used trehalose to stimulate greater levels of autophagy, and showed a reduction in the level of degeneration expected in their brains. Like many animal studies, the mice here were engineered to develop a form of neurodegeneration comparatively rapidly, so as to provide a model for assessment of possible treatments at a lower cost:

The accumulation of insoluble proteins is a pathological hallmark of several neurodegenerative disorders. Tauopathies are caused by the dysfunction and aggregation of tau protein and an impairment of cellular protein degradation pathways may contribute to their pathogenesis. Thus, a deficiency in autophagy can cause neurodegeneration, while activation of autophagy is protective against some proteinopathies. Little is known about the role of autophagy in animal models of human tauopathy.

In the present report, we assessed the effects of autophagy stimulation by trehalose in a transgenic mouse model of tauopathy, the human mutant P301S tau mouse ... Autophagy was activated in the brain, where the number of neurons containing tau inclusions was significantly reduced, as was the amount of insoluble tau protein. This reduction in tau aggregates was associated with improved neuronal survival in the cerebral cortex and the brainstem. We also observed a decrease of p62 protein, suggesting that it may contribute to the removal of tau inclusions. ... Our findings provide direct evidence in favour of the degradation of tau aggregates by autophagy. Activation of autophagy may be worth investigating in the context of therapies for human tauopathies.

Pleasantly, the authors paid some attention as to whether providing mice with trehalose causes inadvertent calorie restriction, something that plagues the studies of incautious researchers. The effects of calorie restriction are very strong, and if your prospective treatment happens to make the mice in your study eat less - well, those mice will usually do better than their counterparts, all other things being equal. But here:

Water consumption of the three groups (no treatment, sucrose-treated and trehalose-treated) was similar. Sucrose and trehalose had no impact on the animals' weights or coat aspects, suggesting that the health of the mice was similar among the three groups.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm