Changes in the glucose transporter of brain capillaries.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing mechanistic observations and previously reported case/control comparisons without systematic methodology.
PubMed 1295661 · doi:10.1139/y92-252
What was done
The author reviewed alterations in the density of the GLUT-1 facilitative glucose transporter in brain capillary endothelium, contrasting findings in Alzheimer disease (compared to age-matched controls) with a primary clinical disorder of glucose transport across the blood-brain barrier.
What was found
The abstract reports no numerical metrics or statistical values. It states that cerebral microvessels in Alzheimer disease exhibited a marked decrease in glucose transporter density relative to age-matched controls, with no change in erythrocyte membrane transporter density. In contrast, patients with the primary blood-brain barrier transport defect had decreased GLUT-1 density in erythrocyte membranes.
Why it matters
The distinction suggests that brain microvascular GLUT-1 reduction in Alzheimer disease is a consequence of decreased cerebral glucose metabolism rather than the primary cause, while primary transport defects present with systemic erythrocyte GLUT-1 abnormalities.
Limits
The abstract provides no sample sizes, patient characteristics, experimental protocols, or quantitative statistical data. As a narrative review, it represents descriptive synthesis and expert opinion rather than primary clinical evidence.
Cited by
- supports GLUT1 is the primary glucose transporter at the blood-brain barrier and is significantly reduced in postmortem brain vessels of Alzheimer's patients.