Sleep deprivation may speed up development of Alzheimer’s disease.
Read more
Category: neuroscience – Page 917
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).
Read more
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.
Read more
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.
Read more
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
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.
Read more
European nations see biggest increases in use of stimulants such as Ritalin by people seeking brain-boosting effects.
- By Arran Frood, Nature magazine on July 6, 2018
Read more
Marvin Minsky was one of the founding fathers of artificial intelligence and co-founder of the Massachusetts Institute of Technology’s AI laboratory.
Abstract for scientists
Neuro cluster Brain Model analyses the processes in the brain from the point of view of the computer science. The brain is a massively parallel computing machine which means that different areas of the brain process the information independently from each other. Neuro cluster Brain Model shows how independent massively parallel information processing explains the underlying mechanism of previously unexplainable phenomena such as sleepwalking, dissociative identity disorder (a.k.a. multiple personality disorder), hypnosis, etc.
Abstract for non-scientists
Neuro cluster Brain Model is the brain model based on neuroscience which demystifies, reveals and explains all religious and occult phenomena. Millions of people have experienced various religious and occult phenomena however skeptical scientists deny even the existence of such phenomena. The denial of the phenomena is not the solution because the denial provides no explanation why so many people claim to have experienced various religious and occult phenomena. Instead of denial the scientific explanation of underlying mechanisms is needed. Neuro cluster Brain Model provides the scientific explanation of underlying mechanisms of religious and occult phenomena. Neuro cluster Brain Model succeeds where other scientific models fail. For the first time ever all religious experiences (communication with Gods, angels, demons, etc) and psychic powers (mediumship, psychography, telepathy, etc) are revealed and explained in the scientific way.
The workings of memory and learning have yet to be clarified, especially at the neural circuitry level. But researchers at Uppsala University have now, jointly with Brazilian collaborators, discovered a specific brain neuron with a central role in learning. This study, published in Neuron, may have a bearing on the potential for counteracting memory loss in Alzheimer’s disease.
When a person with dementia forgets having just eaten dinner, it is due to hippocampus damage. In contrast, the same person can describe in vivid detail a fishing trip to Norway 40 years ago. Both cases entail the use of episodic memory, the brain’s storage of events in which we have been personally involved. Dementia diseases impair the ability to form new memories, especially of events since the onset of the disease.
Researchers at Uppsala University have now, jointly with Brazilian colleagues, found certain neurons in the brain that play a crucial part in learning. The same research group had previously discovered ‘gatekeeper cells’ or, in technical parlance, OLM (Oriens-lacunosum moleculare) cells. These are located in the hippocampus, the brain area known to be active in forming new memories. The new findings from Klas Kullander’s research group show that OLM cells’ activity affects the encoding of memories in the brain.
Read more