Supplemental ketones may fight Alzheimer's disease.

Original title: Supplementing ketones or fighting Alzheimer's disease
A mouse model study published in the Journal of Neuroscience, journal of the American Academy of Neuroscience, showed that a decrease in protective protein levels led to a decrease in the number of inhibitory intermediate neurons in Alzheimer's mice- GABA neurons, which in turn caused abnormal neuronal network activity in mice, while dietary interventions to supplement ketones helped restore the protein levels and inhibit neurone network activity in mice.
impairment of mitochondrial function and abnormal neural network activity are important early events in the pathogenesis of Alzheimer's disease, it is not clear how mitochondrial changes cause abnormal activity in neuron circuits. This time, researchers at the U.S. National Institutes of Health examined the role of mitochondrial deacetylase 3 (SIRT3), a protein that maintains mitochondrial function and protects neurons, in the pathogenesis of Alzheimer's disease.
study, researchers genetically engineered to lower SIRT3 levels in mice with Alzheimer's disease. They found that mice with less than one dose of SIRT3 lost GABA neurons in the cerebral cortex, were more likely to overexcite their neural networks, have more severe seizures and have higher mortality rates than those in the control group. But after feeding the mice ketone-rich foods, the researchers found that their SIRT3 levels increased, the number of seizures decreased significantly, and the mortality rate decreased.
researchers point out that GABA-enabled neurons play an important role in suppressing nerve activity in the brain, and by protecting mitochondrial function, SIRT3 can reduce the effect of beta-amyloid proteins on neurons in alzheimer's mice. Their study showed that lower SIRT3 levels increased the loss of GABA energy neurons in Alzheimer's mice, causing their neural networks to overexcite, while increasing SIRT3 levels through the intake of ketone-rich foods may be an effective intervention to protect GABA energy neurons and delay the progression of Alzheimer's disease.
.