Reversing Alzheimer’s gene blockade can bring back memory

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Breaking a ‘gene blockade’ could pave the way for restoring memory loss and other cognitive functions in patients suffering from Alzheimer’s disease, a new study has suggested.

Researchers have shown that an enzyme overproduced in the brains of Alzheimer’s patients creates a barrier that shuts off genes essential to form new memories.

Furthermore, by inhibiting that enzyme in mice, the MITneuroscientists were able to reverse Alzheimer’s symptoms.

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How significant are developments in making Alzheimer’s brain cells in the lab?

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Dementia has been described as a “time bomb” in society. As more people are living longer, more are being affected by the illness which slowly but surely annihilates brain function.

More than 750,000 people in the UK already have dementia, forecasts say there will be one million dementia patients by 2021 and 1.5 million by 2051. The cost to health services and the economy is already put at more than £20bn each year.

However, the scale of the problem is in stark contrast to the level of understanding. Alzheimer’s disease is the most common form of dementia, yet the cause is unknown and there is no cure.

When it comes to studying dementia you cannot simply take samples of brain tissue from patients to understand what is going on or to test treatments. Research requires good “models” of the disease instead, something many scientists would argue are not good enough.

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Flu may boost Alzheimer’s risk, research suggests

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When we come down with the flu, we might think the worst is over after a week of a sore throat and body aches. But such viral infections may have lasting, unseen effects on the brain, emerging research suggests.

Viruses such as influenza and herpes may leave brain cells vulnerable to degeneration later in life, and increase the risk of developing diseases such as Alzheimer’s and Parkinson’s, research suggests. That’s because these the viruses can enter the brain and trigger an immune response — inflammation — which can damage brain cells.

Viruses and other sources of inflammation “may be initiating factors in some of the most common neurological diseases,” said Dr. Ole Isacson, professor of neurology at Harvard Medical School, who discussed the topic in an article published today (Feb. 15) in the journal Science Translational Medicine.

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Alzheimer’s: Trouble sleeping could affect memory later on, study finds

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People who have trouble sleeping may be at higher risk of developing memory problems, new research shows.

People who woke frequently in the night had a higher risk of developing Alzheimer’s disease, according to work to be presented at the American Academy of Neurology meeting in New Orleans in April.

Other research has shown a link between impaired sleep and multiple-personality disorder, as well as other forms of dissociation.

And research in mice has shown that disrupted sleep can actually cause an increase in the buildup of amyloid plaque in the brain — buildup that happens years before any outward symptoms of Alzheimer’s occur.

To see whether disrupted sleep affected humans, the researchers took 100 patients, half of whom had a family history of Alzheimer’s, and monitored their sleep patterns for 14 days. They found that even though participants spent about eight hours in bed, on average, they spent only about 6.5 hours sleeping, because they woke up repeatedly during the night.

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Alzheimer’s path found by Columbia researchers

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Columbia University researchers have made a surprising discovery about how Alzheimer’s disease appears to spread in the brain, a finding that could one day lead to early treatment for the memory-robbing disease.

The researcher’s findings – published last week in the journal PLoS One – answered a question that had stumped scientists for 25 years: does Alzheimer’s pop up independently in different parts of the brain or does it spread in a predictable pattern from one specific place in the brain to another.

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Hope For Early Alzheimer’s Test In Spinal Fluid

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New research led by Nottingham University in the UK suggests abnormal levels of seven proteins in spinal fluid could be markers for the early stages of Alzheimer’s disease, raising hopes of a test for a disease that is difficult to diagnose at the beginning. The researchers write about their findings in the Journal of Alzheimer’s Disease.

Study co-author Dr Kevin Morgan, professor of Human Genomics and Molecular Genetics at Nottingham, told the press on Tuesday that the findings are “a new lead for improving early diagnosis of Alzheimer’s disease”.

An early diagnosis of Alzheimer’s disease would help people prepare for the future and also enable them to be involved in clinical trials at a much earlier stage of the disease, when treatments are more likely to show positive results, he added.

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