Creutzfeldt-Jakob disease

Creutzfeldt-Jakob disease (CJD) that had been often called ‘mad cow disease’ in the popular press is a degenerative human brain disease that is terminal. It features a number of commonalities of Alzheimer’s disease mainly because it commences with an accelerated development of memory difficulties; behavioral changes such as paranoia, obsessive-compulsive signs and psychosis; inadequate balance and falls along with vision disorders. At a later time the symptoms progress to dementia and automatic jerky movements. CJD is a great deal more faster in its advancement when compared to Alzheimer’s disease and they quickly end up in a coma with close to 70% of individuals having Creutzfeldt-Jakob disease dying inside of a year of the being diagnosed. The disease was called after the German neurologists Hans Gerhard Creutzfeldt and Alfons Jakob in 1920. The cause of Creutzfeldt-Jakob disease is an infectious type of abnormal proteins that are referred to as prions. Most instances of CJD come about for unidentified reasons with almost 10% are passed down from the individuals mother and father in the autosomal dominant manner. You will find 3 sorts of Creutzfeldt-Jakob disease, sporadic, familial and also acquired. Coming in contact with human brain as well as spinal tissue coming from an infected person may also result in its spread. There is absolutely no data that CJD can spread among individuals via normal connection with an infected individual. Creutzfeldt-Jakob disease has an affect on about 1 individual per million people per year and the onset is frequently close to 60 years of age.

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Finding right drug balance for Parkinson’s patients

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Parkinson’s disease is most commonly treated with levodopa, a drug which alleviates the slowing of bodily movements, called bradykinesia, found in Parkinson’s disease patients.

But the benefits of levodopa wear off as the disease progresses. The relationship between its dosage and its effectiveness becomes fuzzy, and high doses can result in dyskinesia, which are involuntary and uncontrollable movements.

To better understand the underlying reasons behind these effects, researchers from the Université de Montréal, University of Bologna, and University of Ottawa created a model of the interactions between levodopa, dopamine, and the basal ganglia, an area of the brain that plays a crucial role in Parkinson’s disease. They discuss their findings in the journal Chaos, from AIP Publishing.

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Study may show why MS patients develop progressive disability

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Did you know multiple sclerosis (MS) means multiple scars? New research shows that the brain and spinal cord scars in people with MS may offer clues to why they developprogressive disability but those with related diseases where the immune system attacks the central nervous system do not.

In a study published in Neurology, Mayo Clinic researchers and colleagues assessed if inflammation leads to permanent scarring in these three diseases:

MS.
Aquaporin-4 antibody positive neuromyelitis optica spectrum disorder (AQP4-NMOSD).
Myelin oligodendrocyte glycoprotein antibody associated disorder (MOGAD).

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In many cases, MS starts long before the diagnosis

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Persons suffering from the autoimmune disease multiple sclerosis can develop various neurological symptoms caused by damage to the nervous system. Especially in early stages, these may include sensory dysfunction such as numbness or visual disturbances. In most patients, MS starts with recurring episodes of neurological disability, called relapses or demyelinating events. These clinical events are followed by a partial or complete remission. Especially in the beginning, the symptoms vary widely, so that it is often difficult even for experienced doctors to interpret them correctly to arrive at a diagnosis of MS.

Above-average numbers of medical appointments

It has been evident for some time, however, that patients with MS show significantly higher numbers of physician visits and hospital admissions even years before the first diagnosis as compared to healthy control persons. In recent years, specialists have seen this pre-diagnosis period as a possible prodromal phase of the disease.

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New study gives clue to the cause, and possible treatment of Parkinson’s Disease

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Researchers from Brain Research Institute, Niigata University, Japan may have unraveled a new approach that could revolutionize the treatment, prevention, and possibly reversal of the damages that could lead to Parkinson’s Disease (PD). This novel finding utilizing the cellular and zebrafish models, demonstrated how the leakage of mitochondrial dsDNA into the cytosol environment of the cell can contribute to the impairment of brain tissue of patients with PD.

Parkinson’s disease is the second most common neurodegenerative disease, and its prevalence has been projected to double over the next 30 years.

These sobering statistics and the quest for PD prognostic marker discovery inspired a team of scientists led by Prof. Hideaki Matsui to build upon previous knowledge that link mitochondrial dysfunction and lysosomal dysfunction to PD. In an interview Prof. Matsui said, “Our results showed for the first time that cytosolic dsDNA of mitochondrial origin leaking and escaping from lysosomal degradation can induce cytotoxicity both in cultured cells, as well as in zebrafish models of Parkinson’s disease.”

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Head injury and concussion in toddlers: Early detection of symptoms is vital

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A research team led by scientists at Université de Montréal has developed a unique observational tool for assessing children up to 5 years of age who have had a concussion. The work is explained in a study published in the Journal of Head Trauma Rehabilitation.

Pediatric traumatic brain injury (TBI) is particularly prevalent in toddlers; they’re more likely to be injured because they have a lower sense of danger and are still developing physically. But parents and clinicians have trouble detecting symptoms of trauma, given the toddler’s limited verbal skills.

“A young child will not tell you that they have a headache or feel dizzy,” said Dominique Dupont, an UdeM postdoctoral student in neuropsychology and first author of the study.

“But assessing post-concussion symptoms is the cornerstone for patient management and follow-up,” she added. “Without documentation, it’s difficult to know whether they’re doing well or not.”

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‘Rejuvenating’ the Alzheimer’s brain

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Alzheimer’s disease is the main cause of dementia and current therapeutic strategies cannot prevent, slow down or cure the pathology. The disease is characterized by memory loss, caused by the degeneration and death of neuronal cells in several regions of the brain, including the hippocampus, which is where memories are initially formed. Researchers from the Netherlands Institute for Neuroscience (NIN) have identified a small molecule that can be used to rejuvenate the brain and counteract the memory loss.

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How injured nerves stop themselves from healing

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Nerves release a protein at the injury site that attracts growing nerve fibers and thus keeps them entrapped there. This prevents them from growing in the right direction to bridge the injury. The research team headed by Professor Dietmar Fischer reports in the journal Proceedings of the National Academy of Sciences (PNAS) from 25. May 2021.

There must be another cause

Three main causes for the inability of injured nerves of the central nervous system, or CNS, to regenerate have been known to date: the insufficient activation of a regeneration program in injured nerve cells that stimulates the growth of fibers, so-called axons; the formation of a scar at the site of injury that is difficult for nerve fibers to penetrate; and an inhibitory effect of molecules in the nerve on regrowing axons. “Although experimental approaches have been found in recent decades to address these individual aspects by therapeutic means, even combinatorial approaches have shown only little success,” says Fischer. “So there must be other yet unknown causes for why nerve fibers in the CNS don’t regenerate.”

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Study shows significant benefit of PolarCap® in recovery from sports-related concussions

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PolarCool AB (publ), a Swedish medical device company focusing on treatment of sports-related traumatic brain injury (TBI) and whiplash, today announced that it has submitted a 510(k) pre-market notification to the U.S. Food and Drug Administration (FDA) for the PolarCap® System.

This submission follows publication of statistically significant clinical results in the scientific journal Concussion, showing clear benefit for use of the PolarCap® System in the treatment of concussions among players of 15 elite Swedish Ice-Hockey teams in the Swedish Hockey Leagues (SHL).

The incidence of sports-related concussions is a significant national health concern in Sweden, as it is here in the U.S., and there is growing evidence that repetitive traumatic brain injury can cause long-term changes in brain structure and function. This is of particular concern in the field of contact sports, such as ice hockey, where available treatment options are limited.

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Damage to white matter is linked to worse cognitive outcomes after brain injury

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A new University of Iowa study challenges the idea that gray matter (the neurons that form the cerebral cortex) is more important than white matter (the myelin covered axons that physically connect neuronal regions) when it comes to cognitive health and function. The findings may help neurologists better predict the long-term effects of strokes and other forms of traumatic brain injury.

“The most unexpected aspect of our findings was that damage to gray matter hubs of the brain that are really interconnected with other regions didn’t really tell us much about how poorly people would do on cognitive tests after brain damage. On the other hand, people with damage to the densest white matter connections did much worse on those tests,” explains Justin Reber, PhD, a UI postdoctoral research fellow in psychology and first author on the study. “This is important because both scientists and clinicians often focus almost exclusively on the role of gray matter. This study is a reminder that connections between brain regions might matter just as much as those regions themselves, if not more so.”

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