Aging and Alzheimer's disease pathology

The number of people with dementia worldwide is predicted to increase to 131.5 million by 2050. When studying dementia, understanding the basis of the neuropathological background is very important. Taking Alzheimer's disease (AD) neuropathology as an example, we know that the accumulation of abnormal structures such as senile plaques and neurofibrillary tangles is a hallmark. Macroscopic atrophy affects the entorhinal area and hippocampus, amygdala, and associative regions of the neocortex. Braak advocates the spread of tau deposits from the entorhinal to associative regions of the neocortex as the disease progresses. If the AD has only tau pathology, the degree and distribution of tau deposition may be associated with clinical symptoms. However, AD is also accompanied by amyloid-β deposition and even atrophy. Although it is possible to make a neuropathological diagnosis of AD from the spread of amyloid and tau depositions, neuropathological abnormal protein accumulation cannot explain all clinical symptoms of AD. There is an ambiguity between clinical symptoms and neuropathological findings. It is important to understand neuropathological findings while understanding that this ambiguity exists. So, for the reader's help, first we briefly explain the changes in the brain with age, and then describe AD as a typical disease of dementia; finally we will describe the diseases that mimic AD for neurologists who are not experts in neuropathology.