Genetic predisposition, family history, and some lifestyle choices are associated with an increased risk of Alzheimer’s and researchers are well aware of the fact that age is one of the greatest risk factors because most people are diagnosed with the condition after 65 years of age.
However, it is unclear, on a molecular level, how aging is associated with Alzheimer’s disease. Several studies have found that there is some faulty glucose metabolism in the brain that causes Alzheimer’s. Also, there have studies showing that mitochondrial dysfunction in the brain cells causes Alzheimer’s.
To dig in deep, researchers from the Salk Institute for Biological Studies and the Scripps Research Institute examined several drugs under conditions that “mimic numerous aspects of old age-associated neurodegeneration and brain pathology, including energy failure and mitochondrial dysfunction.”
The findings of the research appeared in the journal eLife.
Co-author of the research Antonio Currais and colleagues examined two experimental drugs – CMS121 and J147 — which had already shown to have neuroprotective effects in mouse models with Alzheimer’s. The drugs were also found to have the ability to reverse cognitive decline or impairment but the exact mechanisms were unclear.
The experimental drugs are derivatives of plants with medicinal properties.
Currias wrote, “[We] hypothesized that [the compounds] may mitigate some aspects of aging brain metabolism and pathology via a common pathway.”
The researchers said that the experiments found that the group of mice that received the two drugs had a much better memory than those that did not.
They explained that the drugs worked by increasing levels of a chemical known as acetyl-coenzyme A, which improved mitochondrial function, energy production, and cell metabolism. This eventually protected the brain cells from the molecular changes associated with aging.
Co-author of the study Pamela Maher said, “There [were] already some data from human studies that the function of mitochondria is negatively impacted in aging and that it’s worse in the context of Alzheimer’s […]. This helps solidify that link.”
“The bottom line was that these two compounds prevent molecular changes that are associated with aging,” she added. Sharing the future plans, Currais said, “We are now using a variety of animal models to investigate how this neuroprotective pathway regulates specific molecular aspects of mitochondrial biology and their effects on aging and Alzheimer’s.”
