En  este  articulo encuentro   un  soporte fundamental al contemplar  situaciones del deterioro  cognitivo, se  tocan  temas  relevantes como el metabolismoinsulínico y  actividad mitocondria  que precede a la  decadencia propia de  muchas  situaciones  seniles, preseniles y lso síndromes de demencia progresiva.

a Research Center on Aging, Health and Social Services Center–Sherbrooke University Geriatrics Institute, Université de Sherbrooke, Sherbrooke, QC, CanadaReview

Brain fuel metabolism, aging, and Alzheimer’s disease 
M.D., Ph.D.ghTamas Fulop M.D., Ph.D.ab and Stanley I. Rapoport M.D., Ph.D.i
b Department of Medicine, Université de Sherbrooke, Sherbrooke, QC, Canada
c Department of Physiology and Biophysics, Université de Sherbrooke, Sherbrooke, QC, Canada
d Department of Radiobiology and Nuclear Medicine, Université de Sherbrooke, Sherbrooke, QC, Canada
e UMR CNRS-MNHN 7179, Brunoy, France
f Nuclear Medicine Service, ERT-CNRS 5543, Pellegrin Hospital, 33076 Bordeaux, France
g INSERM U897, Bordeaux F-33076
h Université Victor Segalen Bordeaux 2, Bordeaux F-33076, France
i Brain Physiology and Metabolism Section, National Institute of Aging, Bethesda, MD, USA
Received 11 April 2010;  
accepted 28 July 2010.  
Available online 29 October 2010. 

Abstract

Lower brain glucose metabolism is present before the onset of clinically measurable cognitive decline in two groups of people at risk of Alzheimer’s disease---carriers of apolipoprotein E4, and in those with a maternal family history of AD. Supported by emerging evidence from in vitro and animal studies, these reports suggest that brain hypometabolism may precede and therefore contribute to the neuropathologic cascade leading to cognitive decline in AD. The reason brain hypometabolism develops is unclear but may include defects in brain glucose transport, disrupted glycolysis, and/or impaired mitochondrial function. Methodologic issues presently preclude knowing with certainty whether or not aging in the absence of cognitive impairment is necessarily associated with lower brain glucose metabolism. Nevertheless, aging appears to increase the risk of deteriorating systemic control of glucose utilization, which, in turn, may increase the risk of declining brain glucose uptake, at least in some brain regions. A contributing role of deteriorating glucose availability to or metabolism by the brain in AD does not exclude the opposite effect, i.e., that neurodegenerative processes in AD further decrease brain glucose metabolism because of reduced synaptic functionality and hence reduced energy needs, thereby completing a vicious cycle. Strategies to reduce the risk of AD by breaking this cycle should aim to (1) improve insulin sensitivity by improving systemic glucose utilization, or (2) bypass deteriorating brain glucose metabolism using approaches that safely induce mild, sustainable ketonemia.
Keywords: Glucose; Ketones; Brain; Aging; Alzheimer’s disease; PET; Insulin; Cognition; Mitochondria

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