Abstract:
:The presence of the APOE epsilon 4 allele encoding apolipoprotein E4 (apoE4) is the major genetic risk factor for late-onset Alzheimer's disease (AD). However, the molecular and cellular mechanisms by which APOE epsilon 4 renders AD risk are unclear. In this report, we present genetic evidence that an apoE receptor, LRP, may be associated with the expression of late-onset AD. Using a biallelic genetic marker in exon 3 of LRP, late-onset AD cases markedly differed from the control subjects in the distribution of LRP genotypes, and this difference was highly accentuated among AD cases with positive family history of senile dementia. Furthermore, the numbers of neutritic plaques were significantly altered as a consequence of different LRP genotypes in postmortem AD cases. Taken together, our results implicate the pathophysiology of LRP in the expression of late-onset AD.
journal_name
Neurologyjournal_title
Neurologyauthors
Kang DE,Saitoh T,Chen X,Xia Y,Masliah E,Hansen LA,Thomas RG,Thal LJ,Katzman Rdoi
10.1212/wnl.49.1.56subject
Has Abstractpub_date
1997-07-01 00:00:00pages
56-61issue
1eissn
0028-3878issn
1526-632Xjournal_volume
49pub_type
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