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Titolo:
APOLIPOPROTEIN E-EPSILON-4 ALLELES IN CEREBRAL AMYLOID ANGIOPATHY ANDCEREBROVASCULAR PATHOLOGY ASSOCIATED WITH ALZHEIMERS-DISEASE
Autore:
PREMKUMAR DRD; COHEN DL; HEDERA P; FRIEDLAND RP; KALARIA RN;
Indirizzi:
CASE WESTERN RESERVE UNIV,DEPT NEUROL BRB5,10900 EUCLID AVE CLEVELANDOH 44106 CASE WESTERN RESERVE UNIV,DEPT NEUROL BRB5 CLEVELAND OH 44106 CASE WESTERN RESERVE UNIV,DEPT NEUROSCI CLEVELAND OH 44106 CASE WESTERN RESERVE UNIV,DEPT PATHOL CLEVELAND OH 44106
Titolo Testata:
The American journal of pathology
fascicolo: 6, volume: 148, anno: 1996,
pagine: 2083 - 2095
SICI:
0002-9440(1996)148:6<2083:AEAICA>2.0.ZU;2-D
Fonte:
ISI
Lingua:
ENG
Soggetto:
E POLYMORPHISM; E GENOTYPE; BRAIN;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
52
Recensione:
Indirizzi per estratti:
Citazione:
D.R.D. Premkumar et al., "APOLIPOPROTEIN E-EPSILON-4 ALLELES IN CEREBRAL AMYLOID ANGIOPATHY ANDCEREBROVASCULAR PATHOLOGY ASSOCIATED WITH ALZHEIMERS-DISEASE", The American journal of pathology, 148(6), 1996, pp. 2083-2095

Abstract

The presence of apolipoprotein E-epsilon 4 (APOE-epsilon 4) allele has been implicated as a risk factor for Alzheimer's disease (AD). We examined the frequencies of APOE-epsilon 4 alleles in age-matched controls and subgroups of 190 AD subjects exhibiting cerebral amyloid angiopathy (CAA) and other frequently associated lesions. CAA was evident in96% of the AD subjects, which were divided into two groups, one bearing mild or no apparent CAA and the other with moderate to severe CAA. APOE-epsilon 4 allele frequency (48%) in the latter advanced CAA groupwas six times higher than in those who exhibited mild CAA. In the advanced CAA subjects, the occurrence of an epsilon 4 allele was increased by a factor of 17 (95% confidence interval, 7.56 to 38.9). This was despite the fact that neocortical amyloid-beta plaque densities in thetwo groups were similar and that all of the AD subjects had met the accepted neuropathological criteria. We also observed that the degree of CAA severity was greatest in the group of subjects with the epsilon 4/epsilon 4 genotype. The association between CAA and APOE-epsilon 4 was further implicated in two non-AD subjects among neurological controls with severe CAA, These two subjects, both homozygous for the APOE-epsilon 4 allele, were primarily diagnosed as having Creutzfeldt-Jakob disease and Pick's disease is the absence of significant neocortical amyloid deposition. Allele frequency comparisons between neurological control subjects with CAA and those without likewise accorded a strong relationship between the APOE-epsilon 4 allele and the presence of CAA. More remarkably, the epsilon 4 allele frequency was highly associated with AD subjects exhibiting lobar or intracerebral hemorrhage, all of whom had advanced CAA. We observed that 36% of the AD subjects had concomitant cerebrovascular pathology resulting from single infarcts, multiple microinfarcts, ischemic white matter lesions, or petechial hemorrhages. Although the difference in APOE genotype distribution between subjects with and without cerebrovascular lesions did not reach statistical significance, we did note that the frequency of the epsilon 4 allele was significantly higher in subjects with such pathology as compared with those without. However, we found no evidence to suggest that the acquisition of an APOE-epsilon 4 allele or one of the alleles, epsilon 2 or epsilon 3, was a factor in the occurrence of atherosclerosis localized in the basal surface arteries. Analyses of our sample also confirm that there was a lower frequency of the APOE-epsilon 2 allele in AD subjects and that the frequency of the epsilon 4 allele in AD subjects with concomitant diffuse Lewy body disease was intermediate between controls and AD subjects. Our results suggest that the APOE-epsilon 4 allele is a significant factor in the development of CAA in AD and reveal the possibility that APOE is an independent factor in CAA and other vascular abnormalities associated with AD.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/11/20 alle ore 09:57:49