Why Alzheimer's Loves Old Age

Alzheimer's disease usually begins with a decrease in memory, and then other cognitive functions are inhibited. Two substances play a key role in pathogenesis: beta-amyloid plaques and tau-neurofibrillary tangles. The accumulation of neurofibrillary tangles of tau protein indicates the progression of the disease: they are first found in the parts of the brain responsible for memory, and then appear in other areas. Tau protein, more precisely tau aggregates, can probably migrate along nerve fibers and thereby contribute to the spread throughout the brain.

What is the role of aging in the spread of tau protein?

Suzanne Wegmann and colleagues from the German Center for Neurodegenerative Diseases (DZNE) in Berlin, in collaboration with researchers from Harvard Medical School and Massachusetts General Hospital, suggested that tau protein spreads more easily in the aging brain, and this explains the increased susceptibility of older people to Alzheimer's disease.

Using a viral vector (an adapted viral particle), the researchers delivered human tau protein to the brains of mice. As a result, individual brain cells began to produce this protein.

Twelve weeks later, the tau protein content was evaluated. In older mice, human tau protein spread about twice as fast compared to younger animals.

Healthy and pathological tau

Tau protein is present in a healthy soluble form in every neuron of the brain. In Alzheimer's disease, it changes its shape and turns into a pathological form, prone to aggregation into fibrils.

Previously, it was believed that only the pathological form of tau protein spreads from cell to cell. The results of this study show that a healthy version of the protein also spreads in the brain and that this process accelerates in old age. Cells can also be damaged during the accumulation of a large amount of healthy tau protein.

The results of the study raise a number of questions that the group will now study: what processes underlie the acceleration of the spread of tau protein in the aging brain and whether an excess of tau protein is associated with the slow elimination of pathological protein. The answer to these questions will open up new therapeutic possibilities for the treatment of Alzheimer's disease in the long term.

Article by S. Wegmann et al. Experimental evidence for the age dependence of tau protein spread in the brain is published in the journal Science Advances.

Aminat Adzhieva, portal "Eternal Youth" http://vechnayamolodost.ru based on the materials of DZNE: Indications why older people are more susceptible to Alzheimer's disease.