Memory improvement following induced hyperinsulinemia in alzheimer's disease

Dementia of the Alzheimer type (DAT) is accompanied by disruption in glucose regulation and utilization that may contribute to its characteristic memory impairment. Increasing glucose availability by raising plasma glucose improves memory in patients with DAT. Such memory improvement is associated w...

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Bibliographic Details
Published in:Neurobiology of aging 1996, Vol.17 (1), p.123-130
Main Authors: Craft, Suzanne, Newcomer, John, Kanne, Stephen, Dagogo-Jack, Samuel, Cryer, Philip, Sheline, Yvette, Luby, Joan, Dagogo-Jack, Agbani, Alderson, Amy
Format: Article
Language:English
Subjects:
Aged
Alzheimer Disease - metabolism
Alzheimer Disease - physiopathology
Alzheimer Disease - psychology
Alzheimer's disease
Biological and medical sciences
Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases
Fatty Acids - blood
Glucagon - blood
Humans
Hyperglycemia - blood
Hyperinsulinemia
Hyperinsulinism - metabolism
Lactates - blood
Medical sciences
Memory
Memory - physiology
Neurology
Norepinephrine - blood
Psychiatric Status Rating Scales
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Summary:Dementia of the Alzheimer type (DAT) is accompanied by disruption in glucose regulation and utilization that may contribute to its characteristic memory impairment. Increasing glucose availability by raising plasma glucose improves memory in patients with DAT. Such memory improvement is associated with a secondary elevation in plasma insulin levels, raising the question of whether improvement is due to changes in insulin levels, independent of hyperglycemia. Distributions of insulin receptors in the hippocampus and insulin-mediated increases in glucose utilization in entorhinal cortex provide potential mechanisms for such improvement. We show that raising plasma insulin through intravenous infusion while keeping plasma glucose at a fasting baseline level produces striking memory enhancement for patients with DAT. Previous findings of hyperglycemic memory enhancement were also replicated. Patients with DAT also showed abnormal plasma levels of glucoregulatory hormones and metabolites at baseline and during metabolic manipulations. Our findings suggest that neuroendocrine factors play an important role in the pathophysiology of DAT.
ISSN:0197-4580
1558-1497
DOI:10.1016/0197-4580(95)02002-0