An enzyme known for its protective effects on the brain might also protect from Alzheimer’s and Parkinson’s, says a new study available on PLOS Biology.
Researchers from Indiana University have found that the enzyme known as nicotinamide mononucleotide adenylyl transferase 2 (NMNAT2) which is said to shield the brain from oxidative stress can also provide protection against the development of protein clumps which is associated with neurodegenerative diseases like Alzheimer’s, amyotrophic lateral sclerosis (ALS), and Parkinson’s. The built-up of proteins, a process known as proteinopathy, is thought to play a role in the progression of these diseases; an accumulation of the protein called tau in nerve cells, for example, is linked with Alzheimer’s disease.
Co-author Yousuf Ali from Indiana University’s Department of Psychological and Brain Sciences at Indiana explains that high levels of NMNAT2 might be linked with reduced cognitive decline as they found that the enzyme might be curbing proteinopathy. Ali and his team reached these conclusions after examining the brains of over 500 deceased elderly adults; the latter were participants of the Rush Memory and Aging Project when they were alive, and their cognition was evaluated before their death.
Ali and his colleagues analysed the levels of NMNAT2; this enzyme is known to make a compound known as nicotine adenine dinucleotide (NAD) which protects the brain from oxidative stress that is caused by excess nerve cell activity. They then discovered that those adults having greater concentrations of NMNAT2 had a lesser risk of having cognitive decline while the reverse was also true: those with lower levels of the enzyme had a greater risk of having dementia. Therefore, they have concluded that NMNAT2 does not only protect the brain from oxidative stress but also protects it from the impairment of memory and learning.
The team also examined the brains of mice with high levels of the tau protein. This revealed that higher levels of the enzyme in the brain region associated with learning and memory (the hippocampus) also had lower levels of tau as opposed to those mice having lower levels of the enzyme.
The authors write that NMNAT2 levels are “less than 50 percent of control levels”; they, therefore, suggest that magnifying the function of NMNAT2 might preserve cognitive function. Their findings might pave the way to the development of new drugs meant to protect cognition of patients with neurodegenerative diseases.