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Cerebral amyloid β (A beta) and cerebrovascular disease (CSVD) are the main causes of cognitive impairment and dementia.
autopsy studies have shown that AD often coexists with CSVD in patients clinically diagnosed with Alzheimer's disease (AD).
, both increase the risk of Alzheimer's disease, which may be a synergy.
previous studies evaluating the relationship between brain A beta (using PET visible), CSVD and cognition has produced contradictory results.
systematic review found no relationship between brain A and white matter hyperstasy lesions (white matter hyperingens, WMH) in groups with cognitive normality, mild cognitive impairment (MCI), subcortical blood vessels (subcorticalvascular, svMCI, AD, and vascular AD), while in a few studies the higher the brain A beta, the larger the WMH volume.
only one study has shown that brain A beta and WMH interact with the cognition of svMCI individuals.
studies on the relationship between brain atata, lacunes, and cognition have been inconsistent and are mostly confined to individuals with vascular cognitive impairments in the lower cortical layer.
Finally, the correlation between cerebral A-beta and cerebral micro-hemorrhage is difficult to explain because the study was conducted in different sub-groups (cognitive normality, mild cognitive impairment, AD, and A-beta-negative sub-cortical vascular cognitive impairment) without the study evaluating their joint effects on cognition ."
based on these questions, Francis N. Saridin of the National University of Singapore and others included 186 patients with memory impairment, including completely non-cognitive impairment, cognitive impairment but dementia-free no dementia, CIND, AD, and vascular dementia.
to determine brain A-beta by using Pittsburgh compound B-PET global global standard uptake value ratio (SUVR).
small cerebrovascular disease index is mainly white high signal lesions (WMH), infarction, cerebral micro-bleeding (CMBs).
cognitive function was assessed using neuropsytherapy tests.
: In CIND, AD, the decline of SUVR and MMSE was positively related.
, SUVR was associated with decreased cognitive function overall, regardless of age, education, sea mass, and SVD indicators.
in CIND, there is a significant interaction between SUVR and WMH when evaluating the combined effects of SUVR and SVD .
the main significance of this study is that SUVR was associated with poor cognitive function in CIND and AD patients, but only in CIND patients, there was an interaction between SUVR and WMH.
suggests that A-beta and CSVD are independent mutations that may have synergies between A-beta and WMH in CIND individuals.
there is no interaction between A-beta and lacune and micro-bleeding CMB.
, WMH may be licensed as a potentially changeable factor in the preclinical stages of AD to prevent the deterioration of cognitive impairment.
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