A number of previous studies show that insulin is not only produced by the pancreas, but in the brain as well. With insulin resistance, the levels of blood sugar and insulin rise in the bloodstream, but insulin in the brain falls. Shannon Macauley, from Washington University School of Medicine (Missouri, USA), and colleagues infused glucose into the bloodstreams of mice bred to develop an Alzheimer’s-like condition. In young mice without amyloid plaques in their brains, doubling glucose levels in the blood increased amyloid beta levels in the brain by 20%. Repeating the experiment in older mice that already had developed brain plaques, the researchers observed that amyloid beta levels rose by 40%. Further investigation showed that spikes in blood glucose increased the activity of neurons in the brain, which promoted production of amyloid beta. While KATP channels on the surface of brain cells are involved in this neuronal activity, the investigators revealed that an excessive firing in particular parts of the brain can increase amyloid beta production, which ultimately can lead to more amyloid plaques and foster the development of Alzheimer’s disease. The study authors report that: “these results suggest that KATP channel activation mediates the response of hippocampal neurons to hyperglycemia by coupling metabolism with neuronal activity and [interstitial fluid amyloid beta] levels.
Diabetes – Alzheimer’s Link
Macauley SL, Stanley M, Caesar EE, Yamada SA, Raichle ME, Perez R, Mahan TE, Sutphen CL, Holtzman DM. “Hyperglycemia modulates extracellular amyloid-β concentrations and neuronal activity in vivo.” J Clin Invest. 2015 Jun 1;125(6):2463-7.
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