title: Insulin resistance: an emerging link in Alzheimer's disease.
abstract: Relentless progression of Alzheimer's disease (AD) poses a grave situation for the biomedical community to tackle. Agents starting as hot favorites in clinical trials have failed in later stages and it is time we reconsidered our approaches to intervene the disease. Quite some interesting work in the last decade has introduced a new school of thought which factors in neuronal glycemic imbalance as a major component for the development of AD. Insulin resistance in the brain has brought forward subsequent sequelae which might work towards amyloid accretion and/or tau hyperphosphorylation. It is also pointed out that insulin works by distributing iron to neuronal tissue and an insulin resistant state throws it off gear leading to iron overloading of neurons which is ultimately detrimental. A relatively recent investigation finds the role of c-Jun-N-terminal kinase (JNK3) in AD which also seems to bear a link with insulin resistance.
authors.affiliation: Department of Pharmacology, Postgraduate Institute of Medical Education and Research, Research Block B, 4th Floor, Room No. 4043, Chandigarh, 160012, India, drbikashus@yahoo.com.
authors.forename: Bikash
authors.initials: B
authors.lastname: Medhi
authors.forename: Mrinmoy
authors.initials: M
authors.lastname: Chakrabarty
mesh_terms: D000544:Alzheimer Disease / Q000150:complications / Q000503:physiopathology*; D016229:Amyloid beta-Peptides / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000503:physiopathology; D018450:Disease Progression; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology*; D019636:Neurodegenerative Diseases / Q000150:complications / Q000503:physiopathology; D015398:Signal Transduction / Q000502:physiology; D016875:tau Proteins / Q000378:metabolism
chemical_list: D016229:Amyloid beta-Peptides; D016875:tau Proteins