In this review Alzheimer’s infection (AD) has been identified with the statement of amyloid beta (Aβ) peptide plaques in mind tissues that may cause neurodegeneration.1 Stroke, particularly ischemic stroke (IS), has been connected to embolism and small‐vessel disease.2 Despite the distinctive etiopathogeneses proposed for AD and stroke, clinical examinations have shown that the co‐existence of AD and stroke happens more regularly than anticipated by some coincidence, demonstrating a potential connection between the two disorders.3 However, the connection among AD and stroke (especially IS) has not been completely perceived.
Both AD and IS create because of different factors instead of a solitary reason. Proof has been gathering proposing that vascular pathologies (eg, atherosclerosis) are corresponded, and interconnected with neurodegenerative pathologies going before psychological debilitation, AD, and dementia.4 Although obsessive affirmation is missing, stroke‐related vascular conditions (eg, hypertension and heart sicknesses) were discovered to be related with AD development.5, 6 Yet, the relationship between certain vascular danger elements and AD differ by age. That is, middle‐life vascular danger factors, like hypertension, elevated cholesterol, and stoutness, increment late‐life AD risk,7, 8 however the impact of late‐life vascular danger factors on AD will in general be disputable. Thusly, distinguishing which are the common danger factors for both AD and stroke in mature age requires further investigation and would reveal insight into conceivable regular pathophysiologies.
Reference link- https://alz-journals.onlinelibrary.wiley.com/doi/10.1002/alz.12203
