Previous studies have shown that exercise, an active mind and social interaction may help delay the onset of dementia in Alzheimer’s patients, but now a new study indicates environment also plays a key role.
The study, led by Dennis Selkoe, Vincent and Stella Coates Professor of Neurologic Diseases in the HMS Department of Neurology and Brigham and Women’s Hospital, provides specific, preclinical evidence supporting the concept that prolonged and intensive stimulation by an enriched environment—especially regular exposure to new activities—may have beneficial effects in delaying one of the key negative factors in Alzheimer’s disease.
“This part of our work suggests that prolonged exposure to a richer, more novel environment beginning even in middle age might help protect the hippocampus from the bad effects of amyloid beta, which builds up to toxic levels in 100 percent of Alzheimer’s patients,” said Selkoe
Researchers used a wild-type mouse model to evaluate how the environment might affect the progression of Alzheimer’s. Unlike other preclinical models used in Alzheimer’s research, wild-type mice tend to more closely mimic the scenario of disease development in humans under normal environmental conditions, rather than in individuals with a strong genetic predisposition to the disease.
Alzheimer’s disease occurs when amyloid beta protein accumulates and forms so-called senile plaques in the brain. This protein accumulation can block nerve cells in the brain from properly communicating with one another. This may lead to a gradual erosion of an individual’s mental processes, such as memory, attention and the ability to learn, understand and process information.
Selkoe and his team found that prolonged exposure to an enriched environment activated certain adrenalin-related brain receptors. The activity triggered a signaling pathway that prevented the amyloid beta protein from weakening the communication between nerve cells in the hippocampus, which plays an important role in both short- and long-term memory.
The ability of an enriched, novel environment to prevent amyloid beta protein from affecting the signaling strength and communication between nerve cells was seen in both young and middle-aged wild-type mice.
Moreover, the scientists found that exposing the brain to novel activities in particular provided greater protection against Alzheimer’s disease than did just aerobic exercise. According to the researchers, this observation may be due to stimulation that occurred not only physically, but also mentally, when the mice moved quickly from one novel object to another.
“This work helps provide a molecular mechanism for why a richer environment can help lessen the memory-eroding effects of the buildup of amyloid beta protein with age,” said Selkoe. “They point to basic scientific reasons for the apparent lessening of [Alzheimer’s disease] risk in people with cognitively richer and more complex experiences during life.”
This work was supported by the National Institutes of Health, the Massachusetts Alzheimer’s Disease Research Center, the Massachusetts General Hospital Neurology Clinical Trials Units, and the Harvard NeuroDiscovery Center.
Adapted from Brigham and Women’s Hospital news release.
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