Category: In The News

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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