Alzheimer’s Disease (AD) is a disastrous neurological degenerative disease that effects more and more people each year. Cures and treatments for AD have been minimal at best and until recently didn’t show much promise. It was originally thought that the build up of amyloid beta plaques start overwhelming portions of the brain and eventually kill neurons, however, a recent study found that the removal of these plaques from the brain didn’t show in improvement of cognitive functioning in the patients. What instead was found was accumulated amyloid beta oligomers (AβO) causing a synaptotoxin effect.
A new direction of research was observed. The role of insulin in the brain. Until recent years the brain was considered an “insulin-insensitive organ”, but recent research has shown the central nervous system to rely on many insulin actions for potential neuronal survival and other important functions.
Insulin, from the pancreas, travels through the blood stream to the blood brain barrier (BBB) where it crosses and enters the CNS. Here it is known insulin helps regulate brain metabolism by acting on the hypothalamus. Insulin acts on insulin receptors (IR) which are found in various forebrain areas important for memory formation, consolidation, and retrieval. Clearly, insulin signaling is important in memory functioning, and AD has memory disfunction as a primary symptom.
Another recent study found that a build up of AβOs in various areas in the brain could potentially result in a disfunction of IR in neuronal membranes by pushing the IRs intracellular deeming them useless. This would result in a direct cognitive disfunction in whichever area in the brain the IR is associated with, for instance in the hippocampal forebrain would cause memory impairments.
This connection between AD and insulin signaling in the brain opens up a new door for research. It is possible new treatments for AD could arise from the new research of the insulin pathways in the forebrain. Unraveling these mysteries could could reveal powerful therapeutic opportunities for this devastating disease.
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