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New experimental drug to reverse Alzheimer’s disease

The drug acts on a gene recently identified as responsible for making memories in the brain. It is the same gene that, in a research carried out in 2007, helped to restore long-term memory of mice and that improved the learning of new tasks in this animals.

DNANowadays, according to Nature magazine, researchers of the Massachusetts Institute of Technology (MIT) found that drugs that work on the gene HDAC2 (histone deacetylase 2) reverse the effects of Alzheimer’s and boost cognitive function in mice.

“This gene and its protein are promising targets for treating memory impairment”, Li-Huei Tsai, Picower Professor of Neuroscience who is also a Howard Hughes Medical Institute investigator, said. “HDAC2 regulates the expression of a plethora of genes implicated in plasticity – the brain’s ability to change in response to experience – and memory formation”, the investigator explains.

“It brings about long-lasting changes in how other genes are expressed, which is probably necessary to increase numbers of synapses and restructure neural circuits, thereby enhancing memory”, she said.

Same drugs used in the study – called HDAC inhibitors – currently are being tested for treating patients with Huntington’s disease and they are already available in the market to treat some kinds of cancer.

“Furthermore, this finding will lead to the development of more selective HDAC inhibitors for memory enhancement”, Tsai said. “This is exciting because more potent and safe drugs can be developed to treat Alzheimer’s and other cognition diseases by targeting this HDAC specifically”, she adds.

PillsIn the research, scientists treated mice with Alzheimer’s-like symptoms using HDAC inhibitors. HDACs are a family of 11 enzymes that seem to act as master regulators of gene expression.

Although they have been around for a while, HDACs are an exciting and fast growing new area of research because of their recently discovered effect on chromatin: the DNA spools in the centre of the nucleus of each cell.

This is a structure strongly compressed in which transcription of genes do not often happen. However, some types of HDAC open up the chromatin structure which is thought to ease gene transcription that would otherwise not take place when the structure is too tightly packed.

“To our knowledge, HDAC inhibitors have not been used to treat Alzheimer’s disease or dementia”, Tsai points out. “But now that we know that inhibiting HDAC2 has the potential to boost synaptic plasticity, synapse formation and memory formation, in the next step, we will develop new HDAC2-selective inhibitors and test their function for human diseases associated with memory impairment to treat neurodegenerative diseases”.

“The fact that long-term memories can be recovered by elevated histone acetylation supports the idea that apparent memory “loss” is really a reflection of inaccessible memories”, Tsai explains. “These findings are in line with a phenomenon known as ‘fluctuating memories’, in which demented patients experience temporary periods of apparent clarity”.

Parkinson's brainThe researcher adds that though some HDAC inhibitors are on the market as anti-cancer therapeutics, no specific drug targeting HDAC2 yet exists and they will still need about ten years of investigation or more in order to have an inhibitors treatment for human beings with Alzheimer’s disease.

Experts assure that the results of the study are very promising since they offer valuable information about the process of losing memory in Alzheimer’s and other kinds of dementia, and it is one more step in the identification of the genes involved in the risk of developing this disorder.

If the process that triggers and causes dementia can be found, they assure that someday this disease, which affects about 30 million people in the world, will be prevented.

Via:

http://www.bbc.co.uk/mundo/ciencia_tecnologia/2009/05/090507_alzheimer_farmaco_men.shtm

http://web.mit.edu/newsoffice/2009/hdac2-0506.html

http://www.healthday.com/Article.asp?AID=626843

http://www.medicalnewstoday.com/articles/149331.php

COGKNOW is funded by the European Comission within the IST-2005/2006-2.5.11 (Unit H3 - eInclusion) Contract #034025

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