According to new research in mice, a diet rich in ketone—a specific type of fatty acid—can protect neurons from casualty during the development of Alzheimer’s disease. During the early progression of Alzheimer’s disease, the brain is overexcited, probably with the loss of inhibitory or GABAergic—which are interneurons that keep other neurons from signaling excessively. As interneurons need additional energy in comparison to other neurons, they might be more vulnerable to dying when they are subjected to amyloid-beta—the Alzheimer’s disease protein. Seemingly, amyloid-beta has been shown to impair mitochondria by intruding with SIRT3, which is a protein that protects mitochondrial functions and neurons. The study findings were published in the Journal of Neuroscience.
Dr. Aiwu Cheng along with colleagues genetically decreased levels of SIRT3 in mouse prototypes of Alzheimer’s disease. They reported mice having low levels of SIRT3 encountered a much high mortality rate, more aggressive seizures, and elevated interneuron death in correlation to the mice from the control and standard Alzheimer’s disease model. Nevertheless, the mice with lower levels of SIRT3 suffered fewer seizures and were less inclined to die when they consumed a ketone-supplemented diet. The diet also surged levels of SIRT3 in the mice. Elevating SIRT3 levels through ketone intake may be a method to protect interneurons and postpone the development of Alzheimer’s disease.
On a similar note, recently scientists discovered a potential new target to tackle Alzheimer’s disease. Researchers from Temple University’s LKSOM (Lewis Katz School of Medicine) showed that mitochondrial calcium transport remodeling—which is an attempt by cells to balance for signaling energy production and metabolic dysfunction—that is primarily beneficial, eventually becomes maladaptive, increasing declines in mitochondrial function, learning, and memory. The new research was published in the journal Nature Communications. This is the first study to link maladaptive alterations in calcium transport by mitochondria to the development of Alzheimer’s disease.