Stroke: The relationship between A-beta and Tau in cerebrovascular disease and cortological microinfarction

Alzheimer's disease (AD) is the most common cause of dementia and one of the most serious problems facing an ageing population.
according to the International Alzheimer's Report, there were 47 million AD patients worldwide in 2015 and is expected to increase to 131 million by 2050.
pathology of AD is characterized by the highly phosphatized tau protein deposited in neurons to form nerve fiber tangles (NFTs), as well as the accumulation of amyloid β (A beta).
highly phosphate tau protein is also common in neurons, which are closely related to neurons in nerve plaques.
while there is consensus that these pathological changes accumulate throughout the clinical phase of AD, the latest study found that these pathological changes can also be observed in the brain in older people without cognitive impairment.
, the long-term strategy for reducing dementia is to identify disease risk factors early and intervene in the disease process, thereby delaying the onset of the disease.
literature suggests that genetic, psychosocial, vascular and lifestyle risk factors play a role in the development of dementia and AD.
, the most widely accepted is the development of dementia with vascular lesions.
An increasing body of evidence further confirms how vascular lesions lead to cognitive impairment: 1) vascular lesions may be related to the pathogenesis of AD pathology, 2) the correlation between vascular disease and dementia, and 3) vascular risk factors can easily cause individuals to develop vascular dementia and AD.
same time, there is a growing recognition of the importance of microinfarction of the cortical layer caused by vascular lesions in the brain for overall brain health, cognition and Alzheimer's disease.
The extent to which small vascular lesions in the brain are associated with microinfarction and often coexist with Alzheimer's disease is not entirely clear.
to this end, a team from Rush University Medical Center in the United States explored the relationship between small vascular lesions, atherosclerosis, and cerebral amyloid vascular lesions and cortical microinfarction in people with different levels of a beta or tau entanglement.
results were published in the latest issue of stroke.
researchers performed autopsies on 1,489 elderly people from three clinical pathology centers (the average age of death was 89 years old and 67 percent female).
used immunological histification to identify cortical A-beta and tau entanglement burdens in 8 brain regions, and thus to semi-quantitatively grade cerebrovascular disease and assess the presence of cortical microinfarction.
results showed that 17 percent of the elderly had cortical microinfarction, 36 percent had moderate to severe cerebral amyloid vascular pathology, and 34 percent had atherosclerosis.
analysis using logistic regression models determined the interaction between A-beta and tau protein deposition and cerebrovascular disease, indicating that when A-beta and tau protein deposition burden is heavy, atherosclerosis is more associated with cortological microinfarction.
same time, the analysis showed that cerebral amyloid vascular disease also interacted, suggesting a closer association between cerebral amyloid vascular disease and cortological microinfarction in the case of higher A-beta and tau entanglement burden.
results show that small vascular lesions often indicate heavy damage to microvascular tissue when the burden of A-beta or Tau protein deposition is heavy.
also shows a potential link between neurodegeneration and cerebrovascular lesions from the side.
: Kapasi A, et al. Aβ (Amyloid Beta) and Tau Tangle Pathology Modifies the Association Between Small Vessel Disease and Cortical Microinfarcts. Stroke. 2021 Feb 11:STROKEAHA120031073. doi: 10.1161/STROKEAHA.120.031073.MedSci Original Source: MedSci Original Copyright Notice: All noted on this website "Source: Met Medical" or "Source: MedSci Original" text, images and audio and video materials, copyrights are owned by Metz Medicine, without authorization, no media, website or individual may reproduce, authorized to reproduce with the words "Source: Mets Medicine".
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