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Category: neuroscience – Page 895

Groundbreaking research shows that neurological health depends as much on signals sent by the body’s large, leg muscles to the brain as it does on directives from the brain to the muscles. Published today in Frontiers in Neuroscience, the study fundamentally alters brain and nervous system medicine — giving doctors new clues as to why patients with motor neuron disease, multiple sclerosis, spinal muscular atrophy and other neurological diseases often rapidly decline when their movement becomes limited.

“Our study supports the notion that people who are unable to do load-bearing exercises — such as patients who are bed-ridden, or even astronauts on extended travel — not only lose muscle mass, but their body chemistry is altered at the cellular level and even their nervous system is adversely impacted,” says Dr. Raffaella Adami from the Università degli Studi di Milano, Italy.

The study involved restricting mice from using their hind legs, but not their front legs, over a period of 28 days. The mice continued to eat and groom normally and did not exhibit stress. At the end of the trial, the researchers examined an area of the brain called the sub-ventricular zone, which in many mammals has the role of maintaining nerve cell health. It is also the area where neural stem cells produce new neurons.

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Scientists have discovered a “Big Bang” of Alzheimer’s disease – the precise point at which a healthy protein becomes toxic but has not yet formed deadly tangles in the brain.

A study from UT Southwestern’s O’Donnell Brain Institute provides novel insight into the shape-shifting nature of a tau molecule just before it begins sticking to itself to form larger aggregates. The revelation offers a new strategy to detect the devastating disease before it takes hold and has spawned an effort to develop treatments that stabilize tau proteins before they shift shape.

“This is perhaps the biggest finding we have made to date, though it will likely be some time before any benefits materialize in the clinic. This changes much of how we think about the problem,” said Dr. Marc Diamond, Director for UT Southwestern’s Center for Alzheimer’s and Neurodegenerative Diseases and a leading dementia expert credited with determining that tau acts like a prion – an infectious that can self-replicate.

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Nanomaterials that mimic nerve impulses (credit: Osaka University)

A combination of nanomaterials that can mimic nerve impulses (“spikes”) in the brain have been discovered by researchers at Kyushu Institute of Technology and Osaka University in Japan.

Current “neuromorphic” (brain-like) chips (such as IBM’s neurosynaptic TrueNorth) and circuits (such as those based on the NVIDIA GPGPU, or general purpose graphical processing unit) are devices based on complex circuits that emulate only one part of the brain’s mechanisms: the learning ability of synapses (which connect neurons together).

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Scientists at the California Institute of Technology can now assess a person’s intelligence in moments with nothing more than a brain scan and an AI algorithm, university officials announced this summer.

Caltech researchers led by Ralph Adolphs, PhD, a professor of psychology, neuroscience and biology and chair of the Caltech Brain Imaging Center, said in a recent study that they, alongside colleagues at Cedars-Sinai Medical Center and the University of Salerno, were successfully able to predict IQ in hundreds of patients from fMRI scans of resting-state brain activity. The work is pending publication in the journal Philosophical Transactions of the Royal Society.

Adolphs and his team collected data from nearly 900 men and women for their research, all of whom were part of the National Institutes of Health (NIH)-driven Human Connectome Project. The researchers trained their machine learning algorithm on the complexities of the human brain by feeding the brain scans and intelligence scores of these hundreds of patients into the algorithm—something that took very little effort on the patients’ end.

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A disclaimer on the new article that I wrote: while I do think the Beta-amyloid plaque plays a key role in the development of Alzheimer’s disease I do not think it’s the only thing. I’ll be writing more on Alzheimer’s disease as I study more.

The abnormal accumulation β-amyloid peptide is the leading candidate for the cause of Alzheimer’s disease is currently ranked the 6 th leading cause of death in the United States while some statistics claim it may rank as high as the third leading cause of death.

What is Alzheimer’s disease?

Alzheimer’s is a slowly progressive disease that causes the loss of memories and cognitive function. It is the most common form of dementia and accounts for 60 to 80% of cases.

Continue reading “Deletion of BACE 1 Enzyme Reverses The Symptoms of Alzheimer’s” | >

The abnormal accumulation β-amyloid peptide is the leading candidate for the cause of Alzheimer’s disease. Alzheimer’s disease is currently ranked the 6th leading cause of death in the United States while some statistics claim it may rank as high as the third leading cause of death.

What is Alzheimer’s disease?

Alzheimer’s is a slowly progressive disease that causes the loss of memories and cognitive function. It is the most common form of dementia and accounts for 60 to 80% of cases.

Alois Alzheimer is credited as documenting the first published case of “presenile dementia.” Later his colleague Kraepelin would identify it as Alzheimer’s disease.

Present treatments for Alzheimer’s are currently ineffective in reversing the effects of Alzheimer’s disease. For well over a decade research has suggested that the precursor of the β-amyloid is implicated in the BACE1 enzyme. Current BACE1 inhibitory drugs are in development to help patients with Alzheimer’s disease.

Xiangyou Hu, pHd and team generated BACE1 conditional knockout (BACE1fl/fl) mice in order to mimic the inhibition of BACE1 in adults. In order to induce the deletion of BACE1 through genetic modification the team also bred BACE1fl/fl mice with ubiquitin-CreER (a genetic inhibitor) after passing early developmental stages.

Results

The reversal of amyloid deposition was the result of sequential and increased deletion of BACE1 in an adult AD mouse model 5xFAD.

Another significant improvement based upon the reversal of amyloid deposition was in gliosis, which is one of the most prominent features of many diseases of the central nervous system. Gliosis is a process which leads to scarring within the central nervous system. It is well established that neurotic dystrophy is induced by Beta-amyloid plaque.

Thus another result of this reversal saw an improvement in less neurotic dystrophy. Moreover, as determined by experiments of contextual fear conditioning and by long-term potentiation, there was vast improvement in synaptic functions.

The results indicate that the reversal of Beta-amyloid deposition through the inhibition of BACE1 in AD mouse models will provide insight for the proper use of BACE1 inhibitor in human patients.

Journal of Experimental Medicine

Published February 14, 2018

Full Abstract Study

Cerebral small vessel disease (SVD) is one of the most commonly associated causes of age-related dementia and stroke. New research, led by the University of Edinburgh, may have finally uncovered the mechanism by which SVD causes brain cell damage, as well as a potential treatment to prevent the damage, and possibly even reverse it.

SVD is thought to be responsible for up to 45 percent of dementia cases, and the vast majority of senior citizens are suspected of displaying some sign of the condition. One study strikingly found up to 95 percent of subjects between the ages of 60 and 90 displayed some sign of SVD when examined through MRI scans.

The new research set out to examine early pathological features of SVD and found that dysfunction in endothelial cells are some of the first signs of the disease’s degenerative progression. These are cells that line small blood vessels in the brain and, in early stages of SVD, they secrete a protein that impairs production of myelin, a compound essential for the protection of brain cells.

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