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Departments of
* Geriatrics, Medicine, and Psychiatry and
Pathology, University of Arkansas for Medical Sciences, and
Geriatric and Mental Health Research Education and Clinical Centers, Veterans Affairs Medical Center, Little Rock
Correspondence: Professor Sue Griffin, Donald W. Reynolds Center on Aging, 629 South Elm Street, Little Rock, AR 72205. E-mail: griffinsuet{at}uams.edu
Interleukin-1 (IL-1), a key molecule in systemic immune responses in health and disease, has analogous roles in the brain where it may contribute to neuronal degeneration. Numerous findings suggest that this is the case. For example, IL-1 overexpression in the brain of Alzheimer patients relates directly to the development and progression of the cardinal neuropathological changes of Alzheimer’s disease, i.e., the genesis and accumulation of ß-amyloid (Aß) plaques and the formation and accumulation of neurofibrillary tangles in neurons, both of which contribute to neuronal dysfunction and demise. Several genetic studies show that inheritance of a specific IL-1A gene polymorphism increases risk for development of Alzheimer’s disease by as much as sixfold. Moreover, this increased risk is associated with earlier age of onset of the disease. Homozygosity for this polymorphism in combination with another in the IL-1B gene further increases risk.
Key Words: brain • neurodegenerative disease • Down’s syndrome • head injury • aging • epilepsy • genetic risk • immunogenetics
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