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Scientists have replicated human brain cells that develop the telltale structures of Alzheimer s disease for the first time in history, a major step forward in how to study the condition and the search for drugs to treat it.

Until now, the best researchers had to study the disease were mice that had developed an imperfect form of the degenerative illness.

Alzheimer s disease is the most common type of dementia and affects almost 500,000 people in the UK alone. As of 2013, there were an estimated 44.4 million people with dementia worldwide, and Alzheimer s is predicted to affect one in 85 globally by 2050.

Researchers at Massachusetts General Hospital in Boston say the success of their Alzheimer s in a dish study was the suggestion to grow human brain cells in a gel, where they formed networks as in an actual brain.

For the study, they gave the neurons genes for Alzheimer s disease and within weeks, the team saw the formation of clumps, known as plaques, and coils known as tangles – the defining features of the illness.

Researchers used human embryonic stem cells, cells that can become any cell of the body, and grew them into a mixture of chemicals that made them turn into neurons. Then neurons were then given Alzheimer s genes and grew them in wells in petri dishes.

It is hoped the research will allow scientists to test drugs easily and quickly.

This new system – which can be adapted to other neurodegenerative disorders – should revolutionise drug recovery in terms of speed, costs and physiologic relevance to disease, lead researcher Rudolph E. Tanzi said.

Testing drugs in mouse models that typically have brain deposits of either plaques or tangles, but not both, takes more than a year and is very costly, he added.

Without three-dimensional model that recapitulates both plaques and tangles, we now can screen hundreds of thousands of drugs in a matter of months without using animals in a system that is considerably more relevant to the events occurring in the brains of Alzheimer s patients.

The petri dish lacks certain crucial components of the brain such as immune system cells, which appear to contribute to the devastation once Alzheimer s has started. However, the research does allow researchers to test drugs that might prevent the disease in the first place.

It is a giant step forward for the field, Dr P. Murali Doraiswamy, an Alzheimer s researcher at Duke University, told the New York Times. It could dramatically accelerate testing of new drug candidates.

Dr Tanzi is now embarking on a project to test 1,200 drugs on the market and 5,000 experimental ones that have finished the first phase of clinical testing. This project would be impossible using mice, due to its sheer scale.

Dr Sam Gandy, of the Icahn School of Medicine at Mount Sinai in New York, told the Boston Globe that the research was a real game changer and has plans to examine the most powerful gene, ApoE4, which contributes to around half of all cases of the illness. It is not yet known why or how the gene is linked to the disease.

The research was published in the journal Nature.

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