There are now a number of published studies that have revealed that the progression of Alzheimer’s-like pathologies can be slowed down by housing mice or rats in enriched (vs impoverished) environments. I’ll discuss this growing body of literature supporting the prophylactic or rejuvenative power of exercising your brain and body (at least if you’re a small rodent) by just learning new things and having fun every day, in future blogs.

A new twist on this story comes from a study led by Dr. Li-Huei Tsai, a MIT scientist who (with her colleagues) has developed one of the most useful mouse models of Alzheimer’s disease (AD) pathology. At any age, Dr. Tsai can manipulate a gene in a mouse that leads to rapid, large-scale neurodegeneration. At its end stages, that degeneration is marked by the signature “plaques” and “tangles” that characterize AD. In a study reported in an advance online publication of the journal Nature, her group showed that they could induce large-scale pathological changes that result in dramatic brain shrinkage, and a dramatic simplification of neuronal interconnections. As a consequence, not surprisingly, their AD model mice became slow learners with bad memories.

Tsai and colleagues then transferred a group of these far-over-the-hill mice into “enriched” (interesting, challenging, continuosly-changing, learning) environments. With this renewal of exploration and new learning and activity, these AD-model mice recovered their long-term memory and their capacity for new learning to normal or above-normal levels.

The growing body of mice and rat studies that demonstrate clear benefits of new, rich learning experiences have raised many further experimental questions. How, exactly, do these richer environments result in a slower progression of AD pathology? How, exactly, do they account for improved behavioral abilities in rodents that already have considerable on-going pathology? Where, exactly, do benefits stem from, in the multiple facets of the newly elaborated learning experiences of the rodent housed in an “enriched” environment? How, exactly, do these rodent demonstrations that EXPERIENCE MATTERS translate to neurologically beneficial human activities? Since we can organize human training to be far more powerful and efficient in how it engages our brains than are these relatively little-controlled rodent behaviors, can we generate correspondingly MORE powerful prophylactic or rejuvenative effects for we humans, by intensively engaging them in optimal new-experience training paradigms and schedules?

We believe that the answer to this final questions is clearly “yes”.

A final comment: These studies remind us, once again, that the correlation between AD pathology and cognitive impairment is not absolute. Autopsy studies have shown that older individuals can be surprisingly competent and in excellent control, with good cognitive skills and abilities for their age — even while their brains can show very substantial pathology. Moreover, pathology can be surprisingly modest in some individuals who have already slipped a considerable distance down that slippery slope into dementia. While pathological progression is generally “bad news” for an older brain, Dr. Tsai’s studies again remind us that even in these deteriorated, pathological end states, the brain is STILL plastic, and rich new experiences CAN be a basis of very substantial functional recovery.