Dementia including Alzheimer is becoming a more significant problem in our society, which an increasing life expectancy; currently about 10% of the population develop some form of dementia during their lifetime. One form of dementia is Alzheimer that account for 50%-70% of the patients, which is characterized by the appearance of plaques and tangles in the brain that involves the aggregation of a protein named tau. Here, I propose that while tau indeed might be the underlying cause of Alzheimer, its initial aggregation could be a cellular repair-response to shearing of neuronal axons and that Alzheimer, and related tauopathies, are more likely due to inadequate removal of the aggregated protein.
Paper No:
1249
