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Interleukin-1 beta: a common cause of Alzheimer's disease and diabetes mellitus


Holden, RJ and Mooney, PA, Interleukin-1 beta: a common cause of Alzheimer's disease and diabetes mellitus, Medical Hypotheses, 45, (6) pp. 559-571. ISSN 0306-9877 (1995) [Refereed Article]

DOI: doi:10.1016/0306-9877(95)90240-6


Alzheimer disease is characterized by the presence of β-amyloid protein deposits, neurofibrillary tangles and cholinergic dysfunction throughout the hippocampal region. In addition, the hippocampus, hypothalamus and olfactory bulb - the three areas where the insulin receptors are most dense - are also subject to neurodegeneration. The exact cause of the β-amyloid deposits and NFTs is unknown. However, it is our intention to explicate the various pathogenic pathways through which Alzheimer disease arises. Fundamentally, the structural and metabolic damage found in Alzheimer disease is due to sustained elevation of interleukin-1β, a feature which is also found in insulin-dependent diabetes mellitus. Similarly, the β-AP deposits found in the Alzheimer brain share the same molecular structure as the amylin deposits found in the pancreatic beta-cells in non-insulin-dependent diabetes mellitus (NIDDM), and are equally neurotoxic. These, and other pathophysiological parallels, afford some insight into the probable cause of Alzheimer disease and, as such, forms the basis of the causal hypothesis advanced in this paper.

Item Details

Item Type:Refereed Article
Research Division:Biomedical and Clinical Sciences
Research Group:Neurosciences
Research Field:Central nervous system
Objective Division:Health
Objective Group:Other health
Objective Field:Other health not elsewhere classified
UTAS Author:Mooney, PA (Dr Phyllis Mooney)
ID Code:4693
Year Published:1995
Web of Science® Times Cited:15
Deposited By:Health Sciences A
Deposited On:1995-08-01
Last Modified:2011-08-24

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