If Alzheimer’s disease is caused primarily by damaged neurons in the brain, researchers from MIT University in the USA wanted to learn more about the exact cellular processes which cause this and whether it can be reversed?
Well, they have added much needed information to this question by identifying an enzyme in the brain known as ‘HDAC2’ which they confirmed negatively regulates synaptic gene expression and neuronal plasticity.
In other words – they noted that production of this enzyme can actually interfere with learning and memory retention, and thus, in people with Alzheimer’s disease this enzyme is unregulated, so too much of it is produced.
The researchers found that blocking this enzyme in the brains of mice with Alzheimer’s disease can reverse memory loss. How?
The MIT research team discovered a way to target HDAC2 and block its interaction with another binding partner called Sp3.
While things start to get a bit molecular here, their research findings (published in the Journal Cell Reports) found by targeting the HDAC2-Sp3 complex, they could enhance cognitive function in mice without affecting overall HDAC2 function, which may be needed in other brain processes.
Dr Li-Huei Tsai, Director of MIT’s Picower Institute for Learning and Memory and lead researcher on the study, said HDAC2 serves as a master regulator of memory gene expression, suggesting that during Alzheimer’s disease it’s elevated so it causes an epigenetic blockade of the expression of those memory genes
“If we can remove the blockade by inhibiting HDAC2 activity or reducing HDAC2 levels, then we can remove the blockade and restore expression of all these genes necessary for learning and memory,” he said.
This research has now added to a growing body of evidence to suggest that the HDAC2-Sp3 complex has a critical function for neuronal health.
The researchers now believe that they can use this information to develop targeted Alzheimer’s disease treatments for human clinical trials.
We’ll keep you posted on future research in this area.
You can view the original research here