Insulin resistance, inflammation, and cognition in Alzheimer's Disease: Lessons for multiple sclerosis.
J Neurol Sci. 2006 Apr 20
Watson GS, Craft S.
Geriatric Research, Education, and Clinical Center, Veterans Affairs Puget Sound Health Care System; Department of Psychiatry and Behavioral Sciences, University of Washington School of Medicine, Seattle, WA 98108, USA.
Insulin resistance (reduced ability of insulin to stimulate glucose utilization) is common in North American and Europe, where as many as one third of all older adults suffer from prodromal or clinical type 2 diabetes mellitus. It has long been known that insulin-resistant conditions adversely affect general health status.
A growing body of findings suggests that insulin contributes to normal brain functioning and that peripheral insulin abnormalities increase the risk for memory loss and neurodegenerative disorders such as Alzheimer's disease. Potential mechanisms for these effects include insulin's role in cerebral glucose metabolism, peptide regulation, modulation of neurotransmitter levels, and modulation of many aspects of the inflammatory network.
An intriguing question is whether insulin abnormalities also influence the pathophysiology of multiple sclerosis (MS), an autoimmune disorder characterized by elevated inflammatory biomarkers, central nervous system white matter lesions, axonal degeneration, and cognitive impairment. MS increases the risk for type 1 diabetes mellitus. Furthermore, the lack of association between MS and type 2 diabetes may suggest that insulin resistance affects patients with MS and the general population at the same alarming rate. Therefore, insulin resistance may exacerbate phenomena that are common to MS and insulin-resistant conditions, such as cognitive impairments and elevated inflammatory responses.
Interestingly, the thiazolidinediones, which are used to treat patients with type 2 diabetes, have been proposed as potential therapeutic agents for both Alzheimer's disease and MS. The agents improve insulin sensitivity, reduce hyperinsulinemia, and exert anti-inflammatory actions. Ongoing studies will determine whether thiazolidinediones improve cognitive functioning for patients with type 2 diabetes or Alzheimer's disease. Future studies are needed to examine the effects of thiazolidinediones on patients with MS.
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_DocSum
There appears to be frequent overlap between MS and Alzheimer's. The same drugs are often prescribed for Mild Cognitive Impairment in both.
Harvard researcher, Dennis J. Selkoe has been reported in Newsweek as suspecting that insulin might be involved there, too. He thinks that Insulin Degrading Enzyme (IDE) breaks down beta-amyloid as well as insulin, but is preferentially drawn to insulin, thereby leaving the beta amyloid to accumulate in the brain (It is generally accepted as the source of the plaques in Alzheimer's!).
Research on Alzheimer's is definitely something to watch and may be important to MS, too. I try to watch AD because my mother-in-law was affected by it, another AWFUL disease. She died three weeks ago. This has been a sad time--making me appreciate smiles all the more!
But this is not the answer for everyone, not me at least! Since Actos is FDA-approved for diabetes, my doctor allowed me to take it for two months. I saw no change in MS symptoms, but did get the published side effect of edema--swelling of feet and ankles! (I'm still trying to get them back to normal.)
Since I know of no other drugs to reduce insulin (and Marie has convinced me that the balance is TOO delicate to play with!), I am still trying to reduce insulin levels with diet. Two months and no effect yet--I still gurgle in the area of the pancreas!