期刊
ARCHIVES OF NEUROLOGY
卷 57, 期 5, 页码 646-650出版社
AMER MEDICAL ASSOC
DOI: 10.1001/archneur.57.5.646
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资金
- NIA NIH HHS [AG12406] Funding Source: Medline
Deposition of beta-amyloid (A beta), a metabolite of approximately 4 kd of the amyloid precursor protein, is a critical pathological feature in Alzheimer disease. We postulate that deposition reflects an imbalance of A beta synthesis and clearance. Several pathways that impact A beta converge on a single receptor molecule, the low-density lipoprotein receptor-related protein (LRP). This multifunctional receptor is the major neuronal receptor both for apolipoprotein E (apoE, protein; APOE, gene) and for alpha(2)-macroglobulin (alpha(2)M, protein, A2M, gene), and it mediates clearance of apoE/A beta and alpha(2)M/A beta complexes. The LRP also interacts with the amyloid precursor protein itself. In this review, we highlight data that support a role for LRP in A beta metabolism and hypothesize that LRP therefore plays a critical role in Alzheimer disease.
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