beta-amyloid modulation of synaptic transmission and plasticity

Venkitaramani, D. V., Chin, J., Netzer, W. J., Gouras, G. K., Lesne, S., Malinow, R., Lombroso, P. J. (October 2007) beta-amyloid modulation of synaptic transmission and plasticity. Journal of Neuroscience, 27 (44). pp. 11832-11837. ISSN 0270-6474

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Abstract

The sequencing of β amyloid protein (Aβ) in 1984 led to the formulation of the “amyloid hypothesis” of Alzheimer's disease (AD) (Glenner and Wong, 1984). The hypothesis proposed that accumulation of Aβ is responsible for AD-related pathology, including Aβ deposits, neurofibrillary tangles, and eventual neuronal cell death (Tanzi and Bertram, 2005). Within a few years, four groups cloned the amyloid precursor protein (APP) gene from which Aβ is processed (Goldgaber et al., 1987; Kang et al., 1987; Robakis et al., 1987; Tanzi et al., 1987). Linkage analysis mapped the gene to chromosome 21, and mutations in APP were found that led to the inappropriate processing of APP into the Aβ1–42 peptide (Goate et al., 1991; Mullan et al., 1992) (for review, see Tanzi and Bertram, 2005). However, these mutations are responsible for only a small fraction of the early-onset familial AD, and the search began for other genes that might also influence the processing of Aβ. Several novel mutations were identified in the presenilins (Levy-Lahad et al., 1995; Rogaev et al., 1995; Sherrington et al., 1995), and apolipoprotein E4 was identified as a major risk factor for the most frequent form of AD (Strittmatter et al., 1993; Mahley et al., 2006).

Item Type:	Paper
Uncontrolled Keywords:	A beta peptide Alzheimer's disease down syndrome glutamate receptor synaptic plasticity Fyn STEP striatal-enriched tyrosine phosphatase FAMILIAL ALZHEIMERS-DISEASE LONG-TERM POTENTIATION INTRACELLULAR A-BETA PROTEIN TRANSGENIC MICE DOWN-SYNDROME PRECURSOR PROTEIN COGNITIVE DEFICITS MOLECULAR-BASIS TYROSINE PHOSPHORYLATION MISSENSE MUTATIONS
Subjects:	diseases & disorders > mental disorders > delirium dementia cognitive disorders > Alzheimer's disease diseases & disorders > mental disorders > genetic disorders > Down syndrome organism description > animal > mammal > rodent > mouse bioinformatics > genomics and proteomics > genetics & nucleic acid processing > DNA, RNA structure, function, modification > mutations bioinformatics > genomics and proteomics > genetics & nucleic acid processing > protein structure, function, modification > protein types > enzymes > kinase > tyrosine kinase
CSHL Authors:	Malinow, Roberto
Communities:	CSHL labs > Malinow lab
Depositing User:	CSHL Librarian
Date:	October 2007
Date Deposited:	02 Sep 2011 19:00
Last Modified:	10 Apr 2018 20:38
PMCID:	PMC2671021
Related URLs:	Publisher
URI:	http://repository.cshl.edu/id/eprint/15273

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