Boosting Mitochondrial Function Reduces Plaque and Improves Cognitive Function in a Mouse Model of Alzheimer ' s Disease

Mitochondria, the power plants of the cell, suffer a general malaise in older individuals. Their dynamics change and their production of energy store molecules declines. This is distinct and separate from the damage to mitochondrial DNA outlined in the SENS vision for rejuvenation therapies, in that it occurs across all cells rather than in a small but significant number of cells. It is probably a secondary or later consequence of other forms of cell and tissue damage, an inappropriate reaction that makes things worse. This decline in mitochondrial function is implicated in neurodegenerative diseases; the brain requires a great deal of energy to function, and some portion of the changes and symptoms of cognitive decline are due to insufficient energy store production. Researchers here make some inroads to putting numbers to that portion, at least in mice, but the challenge inherent in the use of animal models of Alzheimer's disease is that they are very artificial. Mice don't normally suffer from Alzheimer's, and their neural biochemistry must be altered significantly in order to produce any of the protein aggregates seen in Alzheimer's disease. The current models only recapture a slice of the full human condition, focusing on amyloid aggregation rather than the full biochemistry of the Alzheimer's. Thus there is always the question for any specific finding as to whether it will also apply to humans, or whether it is a quirk of the model, no matter how plausible the as...
Source: Fight Aging! - Category: Research Authors: Tags: Daily News Source Type: blogs