Neurologic disorders

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Epstein-Barr virus may be leading cause of multiple sclerosis

Epstein Barr virus may be leading cause of multiple sclerosis - ویروس اپشتین بار و ام اس

Multiple sclerosis (MS), a progressive disease that affects 2.8 million people worldwide and for which there is no definitive cure, is likely caused by infection with the Epstein-Barr virus (EBV), according to a study led by Harvard T.H. Chan School of Public Health researchers.

Their findings were published online in Science.

“The hypothesis that EBV causes MS has been investigated by our group and others for several years, but this is the first study providing compelling evidence of causality,” said Alberto Ascherio, professor of epidemiology and nutrition at Harvard Chan School and senior author of the study. “This is a big step because it suggests that most MS cases could be prevented by stopping EBV infection, and that targeting EBV could lead to the discovery of a cure for MS.”

MS is a chronic inflammatory disease of the central nervous system that attacks the myelin sheaths protecting neurons in the brain and spinal cord. Its cause is not known, yet one of the top suspects is EBV, a herpes virus that can cause infectious mononucleosis and establishes a latent, lifelong infection of the host. Establishing a causal relationship between the virus and the disease has been difficult because EBV infects approximately 95% of adults, MS is a relatively rare disease, and the onset of MS symptoms begins about 10 years after EBV infection. To determine the connection between EBV and MS, the researchers conducted a study among more than 10 million young adults on active duty in the U.S. military and identified 955 who were diagnosed with MS during their period of service.

Release date: 13 January 2022
Source: Harvard T.H. Chan School of Public Health

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Remembering faces and names can be improved during sleep

Remembering faces and names can be improved during sleep - جایگاه خواب در تقویت حافظه

For those who rarely forget a face, but struggle with names, the remedy for boosting learning may as near as your pillow.

New research by Northwestern University is the first to document the effect reactivating memory during sleep has on face-name learning.

The researchers found that people’s name recall improved significantly when memories of newly learned face-name associations were reactivated while they were napping. Key to this improvement was uninterrupted deep sleep.

The research team found that for study participants with EEG measures (a recording of electrical activity of the brain picked up by electrodes on the scalp) that indicated disrupted sleep, the memory reactivation didn’t help and may even be detrimental. But in those with uninterrupted sleep during the specific times of sound presentations, the reactivation led to a relative improvement averaging just over 1.5 more names recalled.

The study was conducted on 24 participants, aged 18-31 years old, who were asked to memorize the faces and names of 40 pupils from a hypothetical Latin American history class and another 40 from a Japanese history class. When each face was shown again, they were asked to produce the name that went with it. After the learning exercise, participants took a nap while the researchers carefully monitored brain activity using EEG measurements. When participants reached the N3 “deep sleep” state, some of the names were softly played on a speaker with music that was associated with one of the classes.

When participants woke up, they were retested on recognizing the faces and recalling the name that went with each face.

The paper, “Targeted memory reactivation of face-name learning depends on ample and undisturbed slow-wave sleep,” will publish Jan. 12 in the Nature partner journal “NPJ: Science of Learning.”

Release date: 12 January 2022
Source: Northwestern University

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Stopping dementia at the nose with combination of rifampicin and resveratrol

Stopping dementia at the nose with combination of rifampicin and resveratrol - امکان کنترل بیماری آلزایمر از راه بینی

Via drug repositioning, Osaka City University creates combination of rifampicin and resveratrol and have shown in mouse models that the nasal administration improves cognitive function without the negative liver side effects of rifampicin alone.

Researchers from Osaka City University have shown in mice models of Alzheimer’s disease, frontotemporal dementia, and dementia with Lewy bodies, that the intranasal administration of rifampicin and resveratrol in combination is safer and improves cognitive function more than rifampicin alone. The research results are expected to lead to the development of safe and effective nasal spray for the prevention of dementia.

 

The results of this study were published online in the Swiss scientific journal Frontiers in Neuroscience.

Release date: 28 December 2021
Source: Osaka City University

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Triggers of stroke: anger, emotional upset, and heavy physical exertion

Triggers of stroke anger emotional upset and heavy physical exertion - انگشت خشم روی ماشه سکته مغزی

global study co-led by NUI Galway into causes of stroke has found that one in 11 survivors experienced a period of anger or upset in the one hour leading up to it. One in 20 patients had engaged in heavy physical exertion.

The suspected triggers have been identified as part of the global INTERSTROKE study – the largest research project of its kind, which analysed 13,462 cases of acute stroke, involving patients with a range of ethnic backgrounds in 32 countries, including Ireland.

Stroke prevention is a priority for physicians, and despite advances it remains difficult to predict when a stroke will occur. Many studies have focused on medium to long-term exposures, such as hypertension, obesity or smoking. Our study aimed to look at acute exposures that may act as triggers.

The research analysed patterns in patients who suffered ischemic stroke – the most common type of stroke, which occurs when a blood clot blocks or narrows an artery leading to the brain, and also intracerebral haemorrhage – which is less common and involves bleeding within the brain tissue itself.

The research has been published in the European Heart Journal.

Release date: 03 December 2021
Source: National University of Ireland Galway

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ALS therapy should target brain, not just spine

ALS therapy should target brain not just spine - اهمیت توجه به مغز در درمان ای ال اس

The brain is indeed a target for treating ALS (amyotrophic lateral sclerosis), Northwestern Medicine scientists have discovered. This flips a long-standing belief that the disease starts in the spinal motor neurons and any therapy would need to target the spine as the key focus.

A new Northwestern study shows the degeneration of brain motor neurons (the nerve cells in the brain that control movement of the limbs) is not merely a byproduct of the spinal motor neuron degeneration, as had been previously thought. The study was conducted in two mouse models of ALS that represent 90% of all ALS pathologies.

ALS is a swift and fatal neurodegenerative disease that paralyzes its victims.

Upper motor neuron diseases, such as ALS, hereditary spastic paraplegia and primary lateral sclerosis affect more than 250,000 people a year in the U.S. alone. There is no cure and no effective long-term treatment strategy.

This is the first study to clearly reveal the brain motor neuron degeneration is not a consequence of spinal motor neuron degeneration but is independent of the spinal motor neuron degeneration.

The research also is the first to show that the gene UCHL1 is important for maintaining the health of brain motor neurons that are diseased due to two independent underlying causes. One is the accumulation of badly folded proteins and the other is the accumulation of sticky protein clumps inside the cells. These problems are observed in more than 90% of all ALS cases and also in other cases of upper motor neuron diseases.

Northwestern University scientists have previously identified NU-9, the first experimental compound that eliminates the ongoing degeneration of upper motor neurons that become diseased and are a key contributor to ALS. Now, this study reveals the importance and significance of treating upper motor neurons in ALS and identifies the first genetic target.

The next step is to determine the best dose and the best site of injection with respect to improvement of movement and reduction of disease conditions in at least two different ALS disease models. After preclinical toxicology studies, scientists will move to translate these results into a clinical trial, a process that likely will take several years.

The paper was published Dec. 2 in Nature Gene Therapy.

Release date: 03 December 2021
Source: Northwestern University 

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Greater Exposure to Nitrogen Dioxide Linked to Higher Levels of Biomarkers of Alzheimer Disease in the Brain

Greater Exposure to Nitrogen Dioxide Linked to Higher Levels of Biomarkers of Alzheimer Disease in the Brain - نقش آلودگی هوا در تشدید آلزایمر

A study has found an association between air pollution and higher levels of deposition of beta-amyloid protein in the brain and of neurofilament light (NfL) in cerebrospinal fluid.

Investigators from the Barcelonaβeta Brain Research Center (BBRC), the research arm of the Pasqual Maragall Foundation, in collaboration with ISGlobal, have found an association between exposure to air pollution and higher levels of biomarkers of Alzheimer’s disease, particularly in individuals with elevated beta-amyloid deposition in the brain. The results of the study, which was supported by the ”la Caixa” Foundation, have been published in Environment International.

Release date: 16 December 2021
Source: Barcelona Institute for Global Health (ISGlobal)

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SARS-CoV-2 protein interacts with Parkinson’s protein, promotes amyloid formation

SARS-CoV-2 protein interacts with Parkinsons protein promotes amyloid formation - کووید19 و بیماری پارکینسون

Case reports of relatively young COVID-19 patients who developed Parkinson’s disease within weeks of contracting the virus have led scientists to wonder if there could be a link between the two conditions. Now, researchers reporting in ACS Chemical Neuroscience have shown that, at least in the test tube, the SARS-CoV-2 N-protein interacts with a neuronal protein called α-synuclein and speeds the formation of amyloid fibrils, pathological protein bundles that have been implicated in Parkinson’s disease.

In addition to respiratory symptoms, SARS-CoV-2 can cause neurological problems, such as loss of smell, headaches and “brain fog.” However, whether these symptoms are caused by the virus entering the brain, or whether the symptoms are instead caused by chemical signals released in the brain by the immune system in response to the virus, is still controversial. In Parkinson’s disease, a protein called α-synuclein forms abnormal amyloid fibrils, leading to the death of dopamine-producing neurons in the brain. Interestingly, loss of smell is a common premotor symptom in Parkinson’s disease. This fact, as well as case reports of Parkinson’s in COVID-19 patients, made Christian Blum, Mireille Claessens and colleagues wonder whether protein components of SARS-CoV-2 could trigger the aggregation of α-synuclein into amyloid. They chose to study the two most abundant proteins of the virus: the spike (S-) protein that helps SARS-CoV-2 enter cells, and the nucleocapsid (N-) protein that encapsulates the RNA genome inside the virus.

Release date: 14 December 2021
Source: American Chemical Society 

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Are scientists homing in on a cure for Parkinson’s disease?

Are scientists homing in on a cure for Parkinson disease - درمان جدید پارکینسون

A molecule that shows promise in preventing Parkinson’s disease has been refined by scientists at the University of Bath and has the potential to be developed into a drug to treat the incurable neurodegenerative disease.

Parkinson’s disease is characterised by a specific protein in human cells ‘misfolding’, where it becomes aggregated and malfunctions. The protein – alpha-synuclein (αS) – is abundant in all human brains. After misfolding, it accumulates in large masses, known as Lewy bodies. These masses consist of αS aggregates that are toxic to dopamine-producing brain cells, causing them to die. It is this drop in dopamine signalling that triggers the symptoms of Parkinson’s, as the signals transmitting from the brain to the body become noisy, leading to the distinctive tremors seen in sufferers.

Previous efforts to target and ‘detoxify’ αS-induced neurodegeneration have seen scientists analyse a vast library of peptides (short chains of amino acids – the building blocks of proteins) to find the best candidate for preventing αS misfolding. Of the 209,952 peptides screened in earlier work by scientists at Bath, peptide 4554W showed the most promise, inhibiting αS from aggregating into toxic disease forms in lab experiments, both in solutions and on live cells.

In their latest work, this same group of scientists tweaked peptide 4554W to optimise its function. The new version of the molecule – 4654W(N6A) – contains two modifications to the parental amino-acid sequence and has proven to be significantly more effective than its predecessor at reducing αS misfolding, aggregation and toxicity. However, even if the modified molecule continues to prove successful in lab experiments, a cure for the disease is still many years away.

Dr Richard Meade, the study lead author, said: “Previous attempts to inhibit alpha synuclein aggregation with small molecule drugs have been unfruitful as they are too small to inhibit such large protein interactions. This is why peptides are a good option – they are big enough to prevent the protein from aggregating but small enough to be used as a drug. The effectiveness of the 4654W(N6A) peptide on alpha synuclein aggregation and cell survival in cultures is very exciting, as it highlights that we now know where to target on the alpha synuclein protein to supress its toxicity. Not only will this research lead to the development of new treatments to prevent the disease, but it is also uncovering fundamental mechanisms of the disease itself, furthering our understanding of why the protein misfolds in the first place.”

Read full paper in the Journal of Molecular Biology.

Release date: 09 December 2021
Source: University of Bath 

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A diet rich in plant-based products reduces the risk of cognitive impairment in the elderly

A diet rich in plant based products reduces the risk of cognitive impairment in the elderly - رژیم غذایی و آلزایمر

A diet rich in plant products reduces the risk of cognitive impairment and dementia in the elderly. This is the result of a study by the Biomarkers and Nutritional Food Metabolomics Research Group of the Faculty of Pharmacy and Food Sciences of the University of Barcelona (UB) and the CIBER on Frailty and Healthy Aging (CIBERFES).

The paper, published in the journal Molecular Nutrition & Food Research, is led by Cristina Andrés-Lacueva, professor at the Faculty of Pharmacy and Food Sciences and head of the Biomarkers and Nutritional Metabolomics of Food Research Group of the UB and the Biomedical Research Network Center in Frailty and Healthy Aging (CIBERFES), which is also part of the Food Innovation Network of Catalonia (XIA).

The results reveal a protective association between metabolites derived from cocoa, coffee, mushrooms and red wine, microbial metabolism of polyphenol-rich foods (apple, cocoa, green tea, blueberries, oranges or pomegranates) and cognitive impairment in the elderly.

The analysis of plasma samples indicated that some metabolites are related to the progression of cognitive impairment and dementia. As Professor Cristina Andrés-Lacueva explains, “for example, 2-furoylglycine and 3-methylanthine, which are biomarkers of coffee and cocoa consumption, had a protective profile, while saccharin –derived from the consumption of artificial sweeteners– is associated with a damaging role”.

Mercè Pallàs, professor at the Faculty of Pharmacy and Food Sciences and member of the Institute of Neurosciences (UBNeuro) of the UB, stresses that “the study of the relationship between cognitive impairment, the metabolism of the microbiota and food and endogenous metabolism is essential to develop preventive and therapeutic strategies that help to take care of our cognitive health”.

Release date: 09 December 2021
Source: University of Barcelona

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Coffee could lower risk of Alzheimer’s disease

Coffee could lower risCoffee could lower risk of Alzheimer disease - کاهش خطر ابتلا به آلزایمر خبری خوش برای دوستداران قهوهk of Alzheimer disease - کاهش خطر ابتلا به آلزایمر خبری خوش برای دوستداران قهوه

Good news for those of us who can’t face the day without their morning flat white: a long-term study has revealed drinking higher amounts of coffee may make you less likely to develop Alzheimer’s disease.

As part of the Australian Imaging, Biomarkers and Lifestyle Study of ageing, researchers from Edith Cowan University (ECU) investigated whether coffee intake affected the rate of cognitive decline of more than 200 Australians over a decade.

Lead investigator Dr Samantha Gardener said results showed an association between coffee and several important markers related to Alzheimer’s disease.

‘Higher Coffee Consumption Is Associated With Slower Cognitive Decline and Less Cerebral Aβ-Amyloid Accumulation Over 126 Months: Data From the Australian Imaging, Biomarkers, and Lifestyle Study’ was published in Frontiers in Aging Neuroscience.

Release date: 23 November 2021
Source: Edith Cowan University