. Selectively reduced expression of synaptic plasticity-related genes in amyloid precursor protein + presenilin-1 transgenic mice. J Neurosci. 2003 Jun 15;23(12):5219-26. PubMed.

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  1. The header rather than the data come as a surprise, given the fact that APP(V717I) transgenic mice display a robust defect in LTP as well as in cognition (water maze) as early as age three to four months. This is in essence the most "early" phenotype of the APP Tg mice (Moechars et al., 1999) preceding by at least six months any neuropathology or amyloid deposits that become apparent at 10-12 months (Schneider et al., 2001; Dewachter et al., 2002). The present work provides the AD commmunity with a surprisingly short list of genes to analyse, which might contain the molecular players that "occupy early bases."

    References:

    . Early phenotypic changes in transgenic mice that overexpress different mutants of amyloid precursor protein in brain. J Biol Chem. 1999 Mar 5;274(10):6483-92. PubMed.

    . Mutant presenilins disturb neuronal calcium homeostasis in the brain of transgenic mice, decreasing the threshold for excitotoxicity and facilitating long-term potentiation. J Biol Chem. 2001 Apr 13;276(15):11539-44. PubMed.

    . Neuronal deficiency of presenilin 1 inhibits amyloid plaque formation and corrects hippocampal long-term potentiation but not a cognitive defect of amyloid precursor protein [V717I] transgenic mice. J Neurosci. 2002 May 1;22(9):3445-53. PubMed.

    View all comments by Fred Van Leuven