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Altered cell-matrix associated ADAM proteins in Alzheimer disease.

Authors: Gerst, JL  Raina, AK  Pirim, I  McShea, A  Harris, PL  Siedlak, SL  Takeda, A  Petersen, RB  Smith, MA 
Citation: Gerst JL, etal., J Neurosci Res. 2000 Mar 1;59(5):680-4.
Pubmed: (View Article at PubMed) PMID:10686596
DOI: Full-text: DOI:10.1002/(SICI)1097-4547(20000301)59:5<680::AID-JNR11>3.0.CO;2-6

Alterations in cell-matrix 'contact' are often related to a disruption of cell cycle regulation and, as such, occur variously in neoplasia. Given the recent findings showing cell cycle alterations in Alzheimer disease, we undertook a study of ADAM-1 and 2 (A Disintegrin And Metalloprotease), developmentally-regulated, integrin-binding, membrane-bound metalloproteases. Our results show that whereas ADAM-1 and 2 are found in susceptible hippocampal neurons in Alzheimer disease, these proteins were not generally increased in similar neuronal populations in younger or age-matched controls except in association with age-related neurofibrillary alterations. This increase in both ADAM-1 and 2 in cases of Alzheimer disease was verified by immunoblot analysis (P < 0.05). An ADAM-induced loss of matrix integration would effectively "reset" the mitotic clock and thereby stimulate re-entry into the cell cycle in neurons in Alzheimer disease. Furthermore, given the importance of integrins in maintaining short-term memory, alterations in ADAM proteins or their proteolytic activity could also play a proximal role in the clinico-pathological manifestations of Alzheimer disease.


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CRRD Object Information
CRRD ID: 10047127
Created: 2015-07-10
Species: All species
Last Modified: 2015-07-10
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.