Targeting an enzyme that interferes with memory-forming
processes in Alzheimer’s patients can be an effective treatment for memory
loss, according to a new study. A team of scientists from the Massachusetts
Institute of Technology (MIT) in the U.S. found that it may be possible to
reverse Alzheimer’s related memory loss with drugs that selectively impede the
ability of the Histone deacetylase-2 (HDAC2) enzyme to interfere with the
communication between brain cells.
Previously, scientists failed to target HDAC2because the drugs that were used also impeded other roles of the enzyme, causing
toxic side effects.
The new research has shown that blocking a molecule called
sp3 that binds to HDAC2
might effectively stop them both from disrupting the communication between
brain cells that is crucial for memory.
"If we can remove the blockade by inhibiting HDAC2
activity or reducing HDAC2 levels," explains Seniorauthor Prof. Li-Huei Tsai, director of the Picower Institute for Learning
and Memory at MIT, "then we can remove the blockade and restore expression
of all these genes necessary for learning and memory."
For over a decade, Prof. Tsai has been researching the role
that enzymes called HDACs play in memory loss. In2007, she discovered that blocking HDAC activity in mice could reverse
memory loss. There are around a dozen types of HDAC in humans.
Alzheimer's disease is the most common form of dementia,
affecting around 850,000 people in the UK. This neurodegenerative disease
gradually diminishes a person’s ability to remember, think, reason, and make
decisions.
There is no cure for thedisease and scientists do not know the causes of the disease. It is more
common among people over 60 years, but it can affect younger people as well.
The new study focuses on the disruption of a process called
synaptic plasticity, which is thought to be crucial for memory and learning.
Research has revealed that synapses – the connections between
brain cells – are "plastic" and are not fixed as the soldered joints
in electronic circuits.
Scientists define synaptic plasticity as a biological
process whereby synapses change over time, depending on specific patterns of
activity.
Scientists previously tested compounds that inhibit HDAC2,
but most these produced side effects, such as interfering with HDAC1. HDAC1 is
crucial for cell proliferation, especially in red and white blood cells.
Therefore, in this new study, Prof. Tsai and his team sought
to find a way to target only the HDAC2 activity that impedes memory. The team
searched for proteins that help the enzyme to bind to the relevant genes.
To find the diabolical pairing, the researchers examined the
expression of genes in postmortem brain samples taken from people who didn’t
have Alzheimer’s.
Of these samples some brains had high and some had low
levels of HDAC2, which helped the researchers to identify more than 2,000 genes
that might be involved with HDAC2 activity.
Next, a technique called gene knockdown was used
to prevent the expression of HDAC2 and other genes in mice. This narrowed down
the search to a gene that made the protein Sp3.
Fragments of HDAC2 were used to connect with Sp3 in the
mice. This effectively mopped up the proteins and prevented them from forming a
complex with complete HDAC2 enzymes.
This clean-up was useful and it helped restore mice’s nerve
functions, providing evidence that the enzyme and its helper were both required
to latch onto the histones and DNA and prevent them from working.
The study was published in the journal Cell Reports.
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