World Alzheimer's Month: how NAD+ supplements can help combat brain disease symptoms

أعراض مرض الزهايمر

• فقدان الذاكرة
• فقدان المفردات
• التحديات البصرية/المكانية
• صعوبة في إكمال المهام
• تقلبات المزاج

أسباب مرض الزهايمر

مرض الزهايمر والخلل الوظيفي في الميتوكوندريا تركز إحدى النظريات حول سبب المرض على الخلايا العصبية وتراكم البروتين. Neurons live for a very long time and repair themselves regularly, however, in people with Alzheimer’s, beta amyloid plaques (which are intended to aid in the repair of the neurons) clump up and cause the neuron to die off. As time progresses more and more of these plaques can build up and cause brain atrophy. In addition to harmful protein accumulation, Alzheimer’s is associated with dysfunctional mitochondria in brain cells. Without functional mitochondria, a cell will die. And in Alzheimer’s patients, you see increased cell death. This is because the brain’s usual DNA repair activity is impaired in Alzheimer’s disease, leading to inflammation and dysfunction. Studies have shown that dietary supplements of NAD+ led to an increase in NAD+ in the brain, reducing the production of beta amyloid, and slowing the decline of patients’ cognitive function. Many chronic conditions actually begin in cells that aren't metabolising effectively – in other words, these diseases have a mitochondrial basis, with more and more being identified with this cause since the 1970s. However, many of them have been successfully treated with NAD+ supplementation.

NAD+ research

Research led by Dr. Vilhelm A. Bohr at NIH’s National Institute on Aging (NIA) set out to test whether NAD+ supplements could normalize NAD+ levels in the brains of mice and counteract deficits in thinking and memory. The research team first developed a new strain of mice that had the main features of human Alzheimer’s disease, such as the abnormal buildup of the proteins tau and amyloid-beta. NAD+ supplements were added to the mice’s drinking water and they found that after three months, the mice had less DNA damage, lower levels of neuron damage and death, increased production of new neurons, and lower brain inflammation than control mice. They also performed better than control mice on many learning and memory tests, such as a water maze and showed better muscle strength and endurance. The research team also tested human cells from people with and without Alzheimer’s disease. As in the mouse studies, NR decreased DNA damage in the cells from people with Alzheimer’s. It will be really interesting to see how this research progresses in the future and how it may improve the outcomes of Alzheimer’s patients.