Abnormalities of Peptide Metabolism in Alzheimer Disease

Author(s): Mai Panchal, Mohamed Rholam, Noureddine Brakch.

Journal Name: Current Neurovascular Research

Volume 1 , Issue 4 , 2004

Submit Manuscript
Submit Proposal

Abstract:

The steady-state level of peptide hormones represents a balance between their biosynthesis and proteolytic processing by convertases and their catabolism by proteolytic enzymes. Low levels of neuropeptide Y, somatostatin and corticotropin-releasing factor, described in Alzheimer disease (AD), were related to a defect in proteolytic processing of their protein precursors. In contrast the abundance of β-amyloid peptides, the major protein constituents of senile plaques is likely related to inefficient catabolism. Therefore, attention is mainly focused on convertases that generate active peptides and counter-regulatory proteases that are involved in their catabolism. Some well-described proteases such as NEP are thought to be involved in β-amyloid catabolism. The search of other possible candidates represents a primary effort in the field. A variety of vascular risk factors such as diabetes, hypertension and arteriosclerosis suggest that the functional vascular defect contributes to AD pathology. It has also been described that β-amyloid peptides potentiate endothelin-1 induced vasoconstriction. In this review, we will critically evaluate evidence relating proteases implicated in amyloid protein precursor proteolytic processing and β-amyloid catabolism.

Keywords: alzheimer, amyloid peptide, proteolytic processing, catabolism, endothelin-1, vasoconstriction

Rights & PermissionsPrintExport Cite as


Article Details

VOLUME: 1
ISSUE: 4
Year: 2004
Page: [317 - 323]
Pages: 7
DOI: 10.2174/1567202043362117
Price: $58