Alzheimer’s Disease Symptoms Reversed By Researchers

Alzheimer’s Disease Symptoms Reversed By Researchers

Researchers found that the enzyme HDAC2 can represent a new target for Alzheimer’s disease treatment. The study, recently published in Nature, shows that Alzheimer symptoms can be reversed by inhibiting HDAC2, an enzyme associated with memory function. More exactly, HDAC2 is an  overproduced enzyme that prevents storage of new memories in the brain of patients suffering from Alzheimer.

Alzheimer is a degenerative brain disease which primarily affects the elderly.  This disease, also called dementia, is manifested by loss of intellectual abilities, behavioral disorders and speech impairment. Hallmarks of the disease are the senile plaques and neurofibrillary degenerescence. In other words, the brains shrink due to cortex atrophy. In the United States of America, Alzheimer’s affects over 5 million people and is expected that number will double in the next 20 years. Discovery of new therapeutic targets might develop new strategys of treating Alzheimer’s disease. However, Li-Huei Tsai, leader of the research team says it will take at least 10 years to begin to market the new drugs.

Alzheimer

The discovered enzyme actually belongs to deacetylase enzymes family, a group of 11 enzymes that modify histones. By deacetylation, chromatin becomes compacted, and this hampers the process of transcription. By inhibiting this enzyme, chromatin would be less compacted, in other words, the genes in that region would be more likely to be transcribed. Previous studies showed that HDAC2 plays a key role in memory and learning processes. In the new experiment, conducted on mice, it was found that inhibition of this gene makes Alzheimer’s symptoms reversible.

The study showed that HDAC2 is very abundant in the hippocampus, the region of the brain responsible for memory. It was also found that HDAC2 is associated with genes involved in neuronal plasticity, which has an important role in learning and memory. Also, it was found that in affected mice, these genes were much less acetylated and expressed. By using the Short Hairpin RNA molecules Called, the scientists were able to block the HDAC2 in the affected rats. Thus, the acetylation was resumed, and genes with a role in neuronal plasticity could be expressed. Therefore, synaptic activity and cognition function improved significantly.

Furthermore, the study also showed that beta amyloid, one of the markers of Alzheimer’s, increases the production of HDAC2. This explains why drugs that act at the level of beta amyloid plaques had only modest results.