Alzheimer's disease (AD) is the frequent form of dementia in the world. Despite over
100 years of research into the causes of AD, including amyloid and tau protein, the research has
stalled and has not led to any conclusions. Moreover, numerous projects aimed at finding a cure
for AD have also failed to achieve a breakthrough. Thus, the failure of anti-amyloid and anti-tau
protein therapy to treat AD significantly influenced the way we began to think about the etiology
of the disease. This situation prompted a group of researchers to focus on ischemic brain episodes,
which, like AD, mostly present alterations in the hippocampus. In this context, it has been proposed that cerebral ischemic incidents may play a major role in promoting amyloid and tau protein
in neurodegeneration in AD. In this review, we summarized the experimental and clinical research
conducted over several years on the role of ischemic brain episodes in the development of AD.
Studies have shown changes typical of AD in the course of brain neurodegeneration post-ischemia, i.e., progressive brain and hippocampal atrophy, increased amyloid production, and modification of tau protein. In the post-ischemic brain, the diffuse and senile amyloid plaques and the
development of neurofibrillary tangles characteristic of AD were revealed. The above data evidently showed that after brain ischemia, there are modifications in protein folding, leading to massive
neuronal death and damage to the neuronal network, which triggers dementia with the AD phenotype