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.

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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.

The Journal of neuroscience : the official journal of the Society for Neuroscience - 1 May 2002

Dewachter Ilse, Reversé Delphine, Caluwaerts Nathalie, Ris Laurence, Kuipéri Cuno, Van den Haute Chris, Spittaels Kurt, Umans Lieve, Serneels Lutgarde, Thiry Els, Moechars Dieder, Mercken Mark, Godaux Emile, Van Leuven Fred

Abstract excerpt

In the brain of Alzheimer's disease (AD) patients, neurotoxic amyloid peptides accumulate and are deposited as senile plaques. A major therapeutic strategy aims to decrease production of amyloid peptides by inhibition of gamma-secretase. Presenilins are polytopic transmembrane proteins that are essential for gamma-secretase activity during development and in amyloid production. By loxP/Cre-recombinase-mediated...

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PMID: 11978821
PMCID: PMC6758348

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