Brain Glucose Hypometabolism after Perirhinal Lesions in Baboons: Implications for Alzheimer Disease and Aging

Author:

Millien Isabelle123,Blaizot Xavier124,Giffard Cyrille12,Mézenge Florence1,Insausti Ricardo4,Baron Jean-Claude1,Chavoix Chantal13

Affiliation:

1. INSERM U320, Université de Basse Normandie, Caen, France

2. DSV/DRM/UMR CEA, Center Cyceron, Université de Basse Normandie, Caen, France

3. Equipe Universitaire, Université de Basse Normandie, Caen, France

4. Human Neuroanatomy Laboratory, School of Medicine, University of Castilla-La Mancha, Albacete, Spain

Abstract

The authors previously reported that excitotoxic lesions of both the perirhinal and entorhinal cortices in baboons induce remote neocortical and hippocampal hypometabolism reminiscent of that observed in Alzheimer disease (AD), suggesting that disconnection may play a role in AD. Because the cerebral metabolic rate of glucose (CMRglc) was preferentially correlated with perirhinal damage, the area first affected by neurofibrillary tangles in both AD and normal aging, the present series of experiments aimed at assessing the specific metabolic effects of perirhinal lesions. Using PET, CMRglc was measured before surgery and sequentially over the ensuing 10 months. Compared with sham-operated baboons, perirhinal lesions induced significant—albeit late and transient—CMRglc decreases in several brain regions, which significantly correlated with histologic damage for some of these regions. Among them, the temporal and hippocampal regions are metabolically affected after extensive rhinal lesions, in early AD, and aging, while the prefrontal region is affected in aging only. Furthermore, in contrast to AD and rhinal lesions, the posterior cingulate cortex was spared. Both the progressive but significant metabolic effects and specific hypometabolic pattern after perirhinal lesions were confirmed by direct comparisons with previous data obtained after combined lesions of both rhinal areas. Thus, although perirhinal damage appears in itself insufficient to induce sustained CMRglc decreases, it may contribute to the hypometabolic profile of both AD and normal aging, most likely with a stronger contribution in the latter.

Publisher

SAGE Publications

Subject

Cardiology and Cardiovascular Medicine,Neurology (clinical),Neurology

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