Cerebral Metabolic Changes in Alzheimer's Disease: Neurobehavioral Patterns

Abstract

Regional cerebral glucose metabolism was surveyed in 37 Alzheimer''s disease (AD) patients and 21 normal controls using positron emission tomography. Where possible, brain regions were specified according to their neurobehavioral function rather than as anatomically demarcated structures. Absolute metabolic values revealed significant differences (p < 0.05) between AD patients and controls for whole brain and the more superior supratentorial brain slices. Normalized values (region/brain stem) showed the most striking declines (p < 0.001) in the association cortex (heteromodal region -21%; unimodal region -19%) and the primary sensory-motor cortex (-13%), with motor, auditory, and visual areas more affected than somatosensory areas. Limbic and para-limbic systems were equally affected (-14%; -11%; p < 0.001). Thalamus, striatum, cerebellum and brain stem were minimally or not affected. Neurobehaviorally defined hypometabolic regions largely parallel affected areas noted in anatomic and previous metabolic studies, with the possible exception of metabolic deficits in the primary sensory-motor complex. Conceivably, brain areas unaffected morphologically by the pathophysiological processes of AD may become dysfunctional due to a disruption of connectivity between regions.

Voxel-based morphometric study of brain volume changes in patients with Alzheimer’s disease assessed according to the Clinical Dementia Rating score

“…4,8,9,[21][22][23] We did not find any GM volumetric differences in the sensorimotor and visual cortices, consistent with previously published reports. 24,25 GM volume reductions were not found in the lower parietal, cingulate or precuneus areas, even in patients with a CDR score of 2, possibly due to the recruitment of patients over 60 years of age with late-onset AD. One previous study found that patients with early-onset AD showed bilateral reductions in the medial temporal lobes, inferior parietal lobules, the precuneus and perisylvian cortices, the right inferior frontal gyrus and bilaterally in the cingulate cortices, whereas late-onset patients with AD showed atrophy in only the bilateral medial temporal cortices.…”

Similar Ultrastructural Breakdown of Cerebrocortical Capillaries in Alzheimer's Disease, Parkinson's Disease, and Experimental Hypertension: What is the Functional Link?

“…For example, a decreased density of glucose transporter sites supports the last assumption and suggests reduced glucose availability in the affected brain regions 5–7. Hence, the imposed metabolic crisis may be reflected by data indicating decreased cerebral glucose uptake and oxygen utilization in Alzheimer brains 8–10…”

Atherosclerotic Lesions and Mitochondria DNA Deletions in Brain Microvessels as a Central Target for the Development of Human AD and AD‐Like Pathology in Aged Transgenic Mice

“…Mitochondrial abnormalities appear to lead to the energy failure and defective energy metabolism fundamental to AD pathology 46,48‐52,56,90,91. Presently, it is widely accepted that the metabolic defects and vascular abnormalities in AD appear to reduce brain metabolism and are correlated with the severity of AD 1,2,4,6,50,54,56,90–93. For the present study, we have extended our investigation to include the vascular compartment.…”