Is Cerebral Amyloid-β Deposition Related to Post-stroke Cognitive Impairment?

Approximately two-thirds of ischemic stroke patients suffer from different levels of post-stroke cognitive impairment (PSCI), but the underlying mechanisms of PSCI remain unclear. Cerebral amyloid-beta (A beta) deposition, a pathological hallmark of Alzheimer's disease, has been discovered in the brains of stroke patients in some autopsy studies. However, less is known about the role of A beta pathology in the development of PSCI. It is hypothesized that cerebral ischemic injury may lead to neurotoxic A beta accumulation in the brain, which further induces secondary neurodegeneration and progressive cognitive decline after stroke onset. In this review, we summarized available evidence from pre-clinical and clinical studies relevant to the aforementioned hypothesis. We found inconsistency in the results obtained from studies in rodents, nonhuman primates, and stroke patients. Moreover, the causal relationship between post-stroke cerebral A beta deposition and PSCI has been uncertain and controversial. Taken together, evidence supporting the hypothesis that brain ischemia induces cerebral A beta deposition has been insufficient so far. And, there is still no consensus regarding the contribution of cerebral amyloid pathology to PSCI. Other non-amyloid neurodegenerative mechanisms might be involved and remain to be fully elucidated.

Automated summary

The relationship between A beta deposition in the brain and PSCI remains uncertain and controversial, with insufficient evidence supporting the hypothesis that brain ischemia induces cerebral A beta deposition. Other non-amyloid neurodegenerative mechanisms may also be involved in PSCI and require further clarification.