Effect of a dominant-negative form of ADAM10 in a mouse model of Alzheimer's disease.

6533b834fe1ef96bd129e219

RESEARCH PRODUCT

Effect of a dominant-negative form of ADAM10 in a mouse model of Alzheimer's disease.

Falk Fahrenholz Ulrich Schmitt Anja Schroeder

subject

ADAM10 Morris water navigation task Glutamic Acid Stimulation Mice Transgenic ADAM10 Protein Amyloid beta-Protein Precursor Mice In vivo Alzheimer Disease Disintegrin Reaction Time Animals Humans Isoleucine Protein precursor Maze Learning Swimming Metalloproteinase Alanine biology Behavior Animal Chemistry General Neuroscience Age Factors Membrane Proteins Valine General Medicine Cell biology Mice Inbred C57BL Psychiatry and Mental health Clinical Psychology ADAM Proteins Disease Models Animal biology.protein Specific activity Geriatrics and Gerontology Amyloid Precursor Protein Secretases

description

The alpha-secretase cleaves in the non-amyloidogenic pathway the amyloid-beta protein precursor (AbetaPP) within the region of the amyloid-beta peptides to prevent their formation and aggregation in the brain. Members of the ADAM family (a disintegrin and metalloprotease) are the main candidates for physiologically relevant alpha-secretases. We recently demonstrated that overexpression of ADAM10 in mice transgenic for human AbetaPP (ADAM10 x APP[V717I]) alleviated functional deficits related to Alzheimer's disease. To further demonstrate that this is due to the specific activity of alpha-secretase, we characterized mice overexpressing an inactive form of ADAM10 (ADAM10[E384A]; ADAM10-dn). Three lines of mice (controls (C57Bl/6 x FVB), APP[V717I[ transgenics and ADAM10-dn x APP[V717I] double-transgenics) were investigated with respect to learning and memory in the Morris water maze. Double-transgenic mice overexpressing ADAM10-dn behaved similar to APP[V717I] overexpressing mice. This provides further evidence that ADAM10 in vivo by its enzymatic activity is able to counteract cognitive deficits. Stimulation of alpha-secretase activity might thus be a suitable approach to study treatment strategies of Alzheimer's disease.

year	journal	country	edition	language
2009-02-18	Journal of Alzheimer's disease : JAD

10.3233/jad-2009-0952 https://pubmed.ncbi.nlm.nih.gov/19221420

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