Category: Neuroscience

Li-Huei Tsai

Science In Mind

MIT researchers find a drug that helps erase traumatic memories in mice.

For years, neuroscientist Li-Huei Tsai has been unraveling the brain circuits that underlie memory, searching for approaches that might be helpful in treating Alzheimer’s disease. In 2007, the Massachusetts Institute of Technology scientist identified an experimental drug that could restore lost memories in mice. Lately, she has been wondering whether that kind of drug might be useful to help people forget traumatic events that cause fear and anxiety.

In a study published Thursday in the journal Cell, Tsai and colleagues used a single dose of the drug, called an HDAC inhibitor, to help mice extinguish a fearful memory of a traumatic event that took place in the distant past.

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By Carolyn Y. Johnson / Globe Staff

Erasing Traumatic Memories

Erasing traumatic memories

New study identifies drug that could improve treatment of posttraumatic stress disorder.

Nearly 8 million Americans suffer from posttraumatic stress disorder (PTSD), a condition marked by severe anxiety stemming from a traumatic event such as a battle or violent attack.

Many patients undergo psychotherapy designed to help them re-experience their traumatic memory in a safe environment so as to help them make sense of the events and overcome their fear. However, such memories can be so entrenched that this therapy doesn’t always work, especially when the traumatic event occurred many years earlier.

MIT neuroscientists have now shown that they can extinguish well-established traumatic memories in mice by giving them a type of drug called an HDAC2 inhibitor, which makes the brain’s memories more malleable, under the right conditions. Giving this type of drug to human patients receiving psychotherapy may be much more effective than psychotherapy alone, says Li-Huei Tsai, director of MIT’s Picower Institute for Learning and Memory.

Illustration: Christine Daniloff/MIT

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DNA damage may cause ALS

New study finds link between neurons’ inability to repair DNA and neurodegeneration.

Amyotrophic lateral sclerosis (ALS) — also known as Lou Gehrig’s disease — is a neurodegenerative disease that destroys the neurons that control muscle movement. There is no cure for ALS, which kills most patients within three to five years of the onset of symptoms, and about 5,600 new cases are diagnosed in the United States each year.

MIT neuroscientists have found new evidence that suggests that a failure to repair damaged DNA could underlie not only ALS, but also other neurodegenerative disorders such as Alzheimer’s disease. These findings imply that drugs that bolster neurons’ DNA-repair capacity could help ALS patients, says Li-Huei Tsai, director of MIT’s Picower Institute for Learning and Memory and senior author of a paper describing the ALS findings in the Sept. 15 issue of Nature Neuroscience.

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Reversing Alzheimer’s gene ‘blockade’ can restore memory, other cognitive functions

Neuroscientists show that HDAC2 enzyme could be a good target for new drugs.

MIT neuroscientists have shown that an enzyme overproduced in the brains of Alzheimer’s patients creates a blockade that shuts off genes necessary to form new memories. Furthermore, by inhibiting that enzyme in mice, the researchers were able to reverse Alzheimer’s symptoms.

The finding suggests that drugs targeting the enzyme, known as HDAC2, could be a promising new approach to treating the disease, which affects 5.4 million Americans. The number of Alzheimer’s victims worldwide is expected to double every 20 years, and President Barack Obama recently set a target date of 2025 to find an effective treatment.

Li-Huei Tsai, leader of the research team, says that HDAC2 inhibitors could help achieve that goal, though it would likely take at least 10 years to develop and test such drugs.

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Unraveling how a mutation can lead to psychiatric illness

MIT neuroscientists show that a gene linked with schizophrenia and bipolar disorder impairs early brain development.

In recent years, scientists have discovered several genetic mutations associated with greater risk of psychiatric diseases such as schizophrenia and bipolar disorder. One such mutation, known as DISC1 — an abbreviation for “Disrupted in Schizophrenia-1” — was first identified in a large Scottish family with high rates of schizophrenia, bipolar disorder and depression.

Studies have since shown that DISC1 mutations can lead to altered brain structure and impaired cognition, but it was unknown exactly how this occurs. A new study from Li-Huei Tsai, director of MIT’s Picower Institute for Learning and Memory, shows that DISC1 mutations impair a specific signaling pathway in neurons that is critical for normal brain development.

In a genetic screen of 750 people — some of whom were healthy and some of whom had psychiatric diseases — the researchers found several common variants of the DISC1 gene. However, even though these mutations disrupted normal brain development, they were not necessarily enough to cause disease on their own.

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