Newly published findings from Wake Forest University School of Medicine researchers shed light on how brain enzymes contribute to memory loss in Alzheimer's patients, which could guide more effective drug treatments for the disease that affects 6.7 million Americans.
The findings are detailed in a mini-review led by Dr. Tao Ma, M.D., Ph.D., professor in the department of Internal Medicine-Gerontology and Geriatric Medicine and the Center for Health Aging and Alzheimer’s Prevention at Wake Forest School of Medicine, published Tuesday in the journal Brain Medicine.
The paper looks at how the brain’s energy-sensing enzyme AMP-activated protein (AMPK) contributes to symptoms of Alzheimer’s disease. AMPK works as a thermostat for brain cells’ energy and regulates protein production needed for synapses to strengthen and support energy. If not regulated properly, learning and memory can suffer.
In the review, researchers concluded that two forms of the enzyme (AMPKa1 and AMPKa2) appear to play different roles in brain health, which could explain why some drug interventions work for some patients and not others.
“Understanding how brain cells manage energy is essential to developing therapies that can protect memory and thinking,” Dr. Ma said. “Our review suggests that not all our thermostats are the same and AMPKa1 and AMPKa2 could have different and even opposing effects on our brain cells. Understanding that difference can help us design better treatments.”
Alzheimer’s is the only disease among the top ten causes of death with no treatment to slow progression with clinical trials showing limited success. A better understanding of the mechanisms of the disease could lead to more effective and targeted treatments, and researchers in the review suggest that compounds that target the AMPK enzymes could help design better treatments.