April 10, 2018

Health Roundup - Alzheimer's Edition

US doctors to be given new definition of Alzheimer's based on biology - not symptoms - which could help spot the disease years earlier

The new framework was released today by the National Institute on Aging that focuses on measurable changes in the brain that set Alzheimer's apart from dementia. Under the proposed research framework, Alzheimer's would be characterized by three factors: evidence of two abnormal proteins associated with Alzheimer's - beta amyloid and tau - and evidence of neurodegeneration or nerve cell death, all of which can be seen through brain imaging or tests of cerebral spinal fluid. It also incorporates measures of severity using biomarkers and a grading system for cognitive impairment. The move will allow doctors to test drugs on people before symptoms show.

Alzheimer's gene has been neutralized in human brain cells for the first time, paving the way for a new treatment

Scientists 'turned off' protein associated with the dementia apoE4 gene. That gene damages nerve cells, with one copy doubling a person's Alzheimer's risk and having two apoE4 copies raises an individual's risk of the disease by 12 times. Researchers warn therapies that are successful in the lab may fail in patients.

This comes after award-winning scientists predicted Alzheimer's will be as manageable as HIV within 10 years. Future dementia treatments will be taken before the condition develops to prevent symptoms rather than attempting to reverse them, according to Professor Michel Goedert, who was involved in discovering the importance of protein plaques in Alzheimer's onset. Professor Goedert, from the University of Cambridge, added: 'Alzheimer's will become something like HIV. 'It's still there but it has been contained or whittled down by drug treatments. It will disappear as a major problem from society.'

Professor Goedert believes drugs under investigation for Alzheimer's often fail due to them being taken too late into the disease's progression. His colleague Professor Bart De Strooper of University College London, with whom he shares the four-million euro Brain Prize money, added: 'The mistakes we have made is the trials is that treatment has been given too late. It's like popping a statin to stop a heart attack."

Absence of a key chemical in the brain, responsible for feeding memory, could be used as an early test for Alzheimer's

The absence of a certain chemical in the brain could be used as an early Alzheimer's test, new research suggests. Dopamine, which regulates movement, 'feeds' a region of the brain responsible for storing memories, known as the hippocampus. When the number of cells producing dopamine reduce, people's memories and abilities to learn new information suffers, which may put them at risk of dementia, according to researchers.  Critics argue further research is required to determine such a test's potential.

Scientists successfully remove Alzheimer's from mice

Certain antibodies may be able to remove Alzheimer’s plaques from the brain, according to new research carried about in mice. As much as 20 years before the symptoms of Alzheimer’s set in, people with the disease begin to develop amyloid beta plaques that build up in the brain and, scientists believe, interfere with neural signals to cause cognitive and memory losses. But researchers at Washington University School of Medicine have developed an antibody that can remove the proteins these plaques are made of altogether, according to their new research. ...The new study experimented with an antibody that matches not the amyloid beta proteins themselves, but a smaller protein contained within them, called APOE. Certain variations of the gene for APOE are the single greatest genetic predictor for Alzheimer as well
We now know some of the key genetics behind the disease, as well as the key biological marker of it in the brain: the amyloid beta protein plaques. These plaques are composed of pieces of protein that come from the fatty membranes that coat neuron cells. Normally, if these fragments break off, naturally occurring enzymes can break them so that they do not have a chance to turn into a clump. For whatever reason, this natural waste removal does not seem to happen in the brains of people with Alzheimer’s. Scientists suspect that as these proteins build up and stick together – either wrapped around neurons or roaming freely through the brain – they block the electrical signals fired across the synapses different parts of the brain try to communicate with one another.

Poor sleep habits create a risk for Alzheimer's disease.'

Poor rest raises the levels of toxic proteins in the brain that can cause memory-robbing disease. A small study, only 20 people,  found a night without sleep increased levels of beta-amyloid in the brain. People with mild memory loss have 21% more beta-amyloid than healthy people while those with Alzheimer's disease have 43% more beta-amyloid. Sleep is vital in clearing away beta-amyloid, which can form clumps in the brain.

The study's lead author, Dr Ehsan Shokri-Kojori, from the National Institutes of Health in Maryland, said: 'Often brain changes seen in animals are not replicated in humans, so this is interesting.'The increase in beta-amyloid we saw in the brains of people who were sleep-deprived is likely to be a harmful process. 'A reasonable prediction based on these results would be that poorer sleep habits create a risk for Alzheimer's disease.'

Prosthetics to Help Memory Loss in Alzheimer's

Scientists at Wake Forest Baptist Medical Center and the University of Southern California (USC) have managed to create and implant a prosthetic system that uses a person’s own memory patterns to facilitate the brain’s ability to create and recall memories. In the pilot study, published in today’s Journal of Neural Engineering, participants’ short-term memory performance showed a 35 to 37 percent improvement over baseline measurements. The research was funded by the U.S. Defense Advanced Research Projects Agency (DARPA).
Posted by Jill Fallon at April 10, 2018 11:30 AM | Permalink