A Systematic Review of Glucose Transport Alterations in Alzheimer's Disease.
Level 4 - case-series / case-control
Systematic review of observational post-mortem, imaging, and animal studies rather than randomized trials
PubMed 34093108 · doi:10.3389/fnins.2021.626636
What was done
A systematic review was conducted across EMBASE and MEDLINE databases (January 1, 1946 to November 1, 2020) examining glucose transporter alterations in Alzheimer's disease across human and rodent studies. In vitro studies, reviews, and letters were excluded.
What was found
Forty-three studies were included (23 human, 20 rodent). Human post-mortem studies consistently showed reductions in GLUT1 and GLUT3 in the hippocampus and cortex. Tracer studies confirmed reduced brain uptake of glucose and glucose-analogs. Rodent studies indicated GLUT1 and GLUT3 reductions occur after amyloid-beta deposition. A small number of studies reported increased GLUT2 and GLUT12, and anti-diabetic medications improved transport capacity. No quantitative effect estimates or statistics were reported in the abstract.
Why it matters
It consolidates evidence that regional glucose hypometabolism in Alzheimer's disease is tied to specific reductions in GLUT1 and GLUT3 downstream of amyloid-beta pathology.
Limits
The review relies primarily on observational post-mortem human tissue and preclinical animal models. The abstract provides qualitative summaries without pooled quantitative meta-analytic estimates.
Cited by
- supports In dementia, brain glucose transport and metabolism face increased resistance and diminished energy utilization.