Functional alterations in Alzheimer's disease: decreased glucose transporter 3 immunoreactivity in the perforant pathway terminal zone.

Abstract

Positron emission tomography (PET) studies measuring glucose utilization have demonstrated cerebral hypometabolism in Alzheimer's disease (AD). The anatomic and biochemical basis for this observation remains unknown. We have examined the distribution in the hippocampal formation of the neuron-specific glucose transporter 3 (Glut3) protein. Using quantitative immunohistochemistry, we find a large reduction (49.5%) in Glut3 immunoreactivity in the outer portion of the molecular layer of the dentate gyrus in AD brains. This region corresponds to the terminal zone of the perforant pathway, whose cells of origin in layer II of the entorhinal cortex are selectively destroyed in AD. Because glucose uptake reflects metabolic demand, these results suggest a decrement of functional activity in the deafferented dentate gyrus granule cells. Generalizing from this observation, decreased glucose uptake seen on PET studies may reflect, in part, decreased glucose transport and utilization in functionally deafferented cortical fields.

• Authors: S D Harr, N A Simonian, B T Hyman
• Journal: Journal of neuropathology and experimental neurology (J Neuropathol Exp Neurol) Vol. 54 Issue 1 Pg. 38-41 (Jan 1995) ISSN: 0022-3069 [Print] England
• PMID: 7815078 (Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)

Chemical References

• Glucose Transporter Type 3
• Monosaccharide Transport Proteins
• Nerve Tissue Proteins
• SLC2A3 protein, human

Topics

• Aged
• Aged, 80 and over
• Alzheimer Disease (metabolism)
• Glucose Transporter Type 3
• Hippocampus (metabolism)
• Humans
• Immunohistochemistry
• Monosaccharide Transport Proteins (metabolism)
• Nerve Tissue Proteins
• Reference Values
• Tissue Distribution