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ISSN: 2161-0460

Journal of Alzheimers Disease & Parkinsonism
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Review Article

Involvement of PKR in Alzheimer’s Disease

Jacques Hugon1,2*, François Mouton-Liger2, Julien Dumurgier1,2, Pauline Lapalus1, Magali Prévôt1, Sandrine Indart1, Jean Louis Laplanche3 and Claire Paquet1,2

1Memory Centre, Saint Louis Lariboisiere Fernand Widal Hospital APHP, University Paris Diderot Paris, France

2Inserm Unit 942, Saint Louis Lariboisiere Fernand Widal Hospital APHP, University Paris Diderot Paris, France

3Department of Biochemistry, Saint Louis Lariboisiere Fernand Widal Hospital APHP, University Paris Diderot Paris, France

Corresponding Author:
Jacques Hugon
Memory Centre, Saint Louis Lariboisiere Fernand Widal Hospital APHP
University Paris Diderot Paris, France
Tel: 33 1 40054313
E-mail: [email protected]

Received date: March 10, 2014; Accepted date: June 30, 2014; Published date: July 30, 2014

Citation: Hugon J, Mouton-Liger F, Dumurgier J, Lapalus P, Prevot M, et al. (2014) Involvement of PKR in Alzheimer’s Disease. J Alzheimers Dis Parkinsonism 4: 154. doi:10.4172/2161-0460.1000154

Copyright: © 2014 Hugon J, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Alzheimer’s disease (AD) is characterized by memory troubles followed by aphasia apraxia and agnosia associated with behavioral disturbances. Neuropathological lesions include senile plaques formed by Aβ peptide, neurofibrillary tangles made of hyperphosphorylated tau and neuronal loss. The cause of AD is unknown but Aβ peptide could be responsible for neuronal degeneration. PKR is a stress and pro-apoptotic kinase that controls protein translation via the phosphorylation of the eukariotic initiation factor 2α (eIF2α). Activated PKR accumulates in affected neurons in AD brains and the phosphorylation of PKR can be induced by Aβ peptide. We have found increased levels of PKR in the cerebrospinal fluid of AD patients and PKR level is a good predictor of the cognitive decline. In addition PKR can modulate the levels of BACE1, an APP cleaving enzyme, and can influence tau phosphorylation. Altogether, PKR represents a potential new biomarker and a valid new therapeutic target for neuroprotection in AD.

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