Scientists at the Salk Institute have found that neurons that are impaired due to cellular aging can be a source of brain inflammation in people with Alzheimer’s disease. The research was published in the journal Cell Stem Cell.
As cells age, they lose their ability to divide and function normally, but they do not die. The molecules they release play an important role in the development of chronic inflammation, which has been linked to cardiovascular disease and cancer. However, earlier scientists believed that these processes occurred in dividing cells, not neurons.
The authors of the new study found that neurons can also age and cause inflammation in the brain, increasing the risk of developing Alzheimer’s disease.
The biologists took skin samples from people with Alzheimer’s disease and transformed the epidermal cells into neurons. They tested these neurons to see if they aged and examined the mechanisms involved in this process.
Scientists have found that as neurons age, they release inflammatory molecules that initiate a series of brain-damaging reactions. Even an “old” neuron can initiate this process, because a cell can make more than a thousand connections with its neighbors. The scientists confirmed their findings by examining signs of aging and gene expression in the brains of 20 people suffering from Alzheimer’s disease.
The authors then tested a treatment cocktail (dasatinib + quercetin) on neurons. Both drugs are used to remove aging cells in the body such as osteoarthritis. The drugs actually reduced the number of aging neurons to normal levels. Therefore, targeting senescent cells may be a useful approach for slow neuroinflammation and neurodegeneration in Alzheimer’s disease.
The researchers noted that the therapeutic cocktail they tested often failed to enter the brain due to the presence of a barrier between the brain’s circulatory system and the rest of the body. Therefore, they believe it is necessary to look for known drugs that have a similar effect but can overcome this barrier.