JNNP: Relationship between lipoprotein E2 genotype and cerebrovascular lesions - 1275 post-brain death studies

Cerebrovascular disease (CVD) is a common common disease of Alzheimer's disease (AD).
in posthumous studies, more than 90 percent of AD patients may have cardiovascular disease, while the number of cases of mixed dementia (AD-CVD) exceeds the number of cases of "pure" AD.
in a large posthumous sample, 27 percent had AD and CVD pathology, while only 3 percent had AD pathology.
1 on the genetic risk of AD and CVD, the relationship between multiple vascular diseases (e.g. lipoprotein 2) and multiple cerebrovascular lesions has not been systematically studied.
the purpose of this paper is to study the relationship between lipoprotein E (APOE) genotype and cerebrovascular disease (CVD).
study of lipoprotein e and CVD pathology has not yet been carried out.
we focused on apoe2, a known neuropulation gene variant that fights Alzheimer's disease.
method: A collection of neuropathological data collected from 39 Alzheimer's centers (ADCs) in the United States was compiled for semi-quantitative scoring through immunobiobiochemistry, tissue chemistry, microscopic observation or visual examination, and appropriate regional examinations.
it includes 1,275 cases with CVD data.
studied 11 lesions of lipoprotein e (APOE) and 1275 cases of cerebrovascular disease (CVD), including obsolescence and recent infarction, haemorrhage, cerebral amyloid vascular disease (CAA) and arteriosclerosis.
the pathology of 39 Alzheimer's center sites were measured in a uniform and semi-quantitative way.
we used χ2 statistics and sequence regression to assess the significantness of the association and to make multiple comparative corrections to Bonferroni.
, NACC does not have a specific measurement of haemorrhage in the large leaf, but we assume that hemorrhage captures most of the cases of haemorrhage in the large leaves in this sample.
we used all the brains in the NACC collected in V.10 for neuropathological CVD measurements, regardless of clinical diagnosis.
result: CAA in 61% of cases in the database.
significantly associated with CAA (χ2 x 188.47, p.lt;0.0001).
E4 is disproportionately related to the number of CAA cases.
no significant differences in sequential regression between lipoproteins E2 and E3 in the same time.
, however, in sequential regression, E2 was significantly associated with a decrease in CAA severity compared to e4 (OR 0.24, 95% CI 0.16-0.34, p.lt;0.0001), 398 cases e2 /e3 or e2/e2 genotype ('e2' carrier), 621 cases were e3 pure thys ('e3' group) and 556 cases were e4/e3 (442) or e4/e4 (114) type ('e4' group).
results showed that the apoe4 allegen significantly increased the risk of CAA.
the presence/non-stratation of CAA, we found that in cases where CAA existed, lipoprotein E2 significantly increased the risk of haemorrhage.
all other connections are negative.
E2/E4 genotypes and CAA cases are significantly higher than E3 (49% CAA present) and other remaining E2 cases (44% CAA present) and are similar to other E3/E4 carrier genotypes in terms of CAA frequency (E2/E4 cases) 76% and 75% of E3/E4 cases) concluded that in the largest study of the pathologically proven effects of lipoprotein E2 on pathologically proven CVD, e2 did not protect any CVD pathology compared to E3 pure thym (including CAA).
for the 1st pathology, e4 is associated with an increase in its severity.
addition, perhaps unexpectedly, in the presence of CAA, E2 significantly increases the risk of acute/subacute haemorrhage.
therefore, although the neuropulatory effect of E2 on amyloid degeneration is limited compared to that of E3/E3 and E4 carriers, it has a significant protective effect on diffuse and neurotisctic amyloid plaques.
Goldberg TE, Huey ED, Devanand DP Associations of APOE e2 genotype with cerebrovascular pathology: a postmortem study of 1275 brainsJournal of Neurology, Neurosurgery and Psygy Published Online First: 04 November 2020. doi: 10.1136/jnnp-2020-323746MedSci Original Source: MedSci Original Copyright Notice: All text, images and audio and video materials on this website that indicate "Source: Met Medical" or "Source: MedSci Original" are owned by Mets Medicine and are not authorized and may not be reproduced by any media, website or individual. "Source: Metz Medicine" shall be indicated at the time of authorization for reprint.
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