Recent research demonstrates that Alzheimer's disease represents a neuro-endocrine disorder that resembles a unique form of diabetes mellitus and progresses with severity of neuro-degeneration.
In their study, to be published in the Journal of Alzheimer's Disease, researchers demonstrate that insulin and its receptors drop significantly in the brain during the early stages of Alzheimer's disease, and that levels decline progressively as the disease becomes more severe, leading to further evidence that Alzheimer's is a new type of diabetes.
Previous studies have shown that reduced glucose utilization and energy metabolism occur early in the course of Alzheimer's disease (AD) and correlate with impaired cognition. Glucose utilization and energy metabolism are regulated by insulin and insulin-like growth factor I (IGF-I), and correspondingly, studies have shown that cognitive impairment may be improved by glucose or insulin administration.
Researchers from the Rhode Island Hospital and Brown Medical School analyzed postmortem brain tissue of 45 patients with a diagnosis of either normal aging or different degrees of Alzheimer's neurodegeneration, termed "Braak Stages."
The study mainly characterizes the abnormalities in insulin and IGF gene expression and receptor binding in brains with different Braak stage severities of AD.
Researchers analyzed insulin and insulin receptor function in the frontal cortex, a major area affected by Alzheimer's, and discovered that with increasing severity of the disease, levels of insulin receptors and the brain's ability to respond to insulin decreased markedly.
The two parallel abnormalities related to insulin in Alzheimer's found were that insulin levels decline as the disease progresses, and, that insulin and its related protein IGF-I lose their ability to bind to corresponding cell receptors, creating a resistance to the growth factors and thus causing cells to malfunction and eventually die.
The authors stress that this could have important implications for treatment of this disease, and that being able to target the disease early, further loss of neurons could be prevented. However, they add that the resistance of its receptors in the brain, along with the loss of insulin will have to be targeted.
The researchers also found that acetylcholine deficiency, a hallmark of the disease, that is also associated with dementia, is linked directly to the loss of insulin and IGF-I function in the brain.