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Regine Humanics Foundation Ltd Publishes The Humanion among doing other things: We do not and shall not accept fundings or contributions from any type, form, manner and layer of Governments of national, international, supra-national or any other type or bodies formed by them nor from rich individuals or bodies or agencies of any kind. This, to us, is as a matter of absolute philosophic principle to ensure our resolute and complete independence. The ways, in which, we invite support from the readers, members of the public and all other individuals and agencies and businesses of any kind, are: a: Voluntary Subscription Payments: b: Voluntary Contributions: c: The Minimal and Symbolic Membership Fees to Our Regineumanics Family: d: Buying a Copy of The Long Walk to Humanics: e: Contributing to Our Events and f: Advertisement in The Humanion. We say it here and invite you for your support and we do not keep asking you on every page your visit to read the materials. You make a conscious, wilful and philosophic choice to Support The Humanion and The Foundation. If, you do: thank you: If, you do not, thank you, too, for reading The Humanion. The world has, apparently, accepted that Capitalism is the High Pinnacle of All Systems and, some still dream that Marxism will rescue humanity from this Killing Mechanism Capitalism, we refuse to subscribe to that and Humanics is the Post-Marxist and Post-Capitalistic World View of What Humanity can be and what it can do and how infinitely better a human condition can be created in a Humanical Society, by eradicating ownership and money and by establishing belongingship in human enterprise, setting all humans at liberty and equality under the rule of law in natural justice with a direct form of democracy, humanics calls it, Humanicsovics, in which, each human soul is her:his own High Representative. In this, Humanics is the Minority Vision and, in this, we do not and can not expect millions and billions of people supporting our vision today but We Whole-Heartedly Believe That ONE DAY This Humanity Shall BE ALL HUMANICAL: By When: We Know Not But This: That Being a Monstrous Killing Mechanism Capitalism IS Unsustainable: But the World Shall Change One Day and Every Change Begins with an Idea, with a Vision: We invite you to Envision the Vision of Humanics and Support The Humanion and The Foundation to Keep Taking Forward the Vision of Humanics for an Infinitely Better Humanity in an Infinitely Better Human Condition for All Humanity Across Mother Earth. Thank You.

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Poetry of Neurology

We are more than our neurons or their combinations, co-relations, conjunctions, functions and interactions, that are conducted through their gap junctions, synapses or action potentials. We are more than the cells, tissues, organs, systems, DNAs, RNAs, genes etc and their ultimate unification into a whole mechanism and system of magnificence. We are an infinity unfolding itself in the name of the human mind which, through the physiology of what on appearance is a human physique, it becomes, dreams, imagines, creates, loves and does human: the most astonishing of all things, that we find on this Universe. All we have to do is to look at its unity off the billion plus expressions of its self and wonder about its endless expressive diversity off the same self in billion plus instances to realise that this human mind is magnificent a thing for the purpose of which the neurology is given to it as the most sophisticated, most elaborately engineered, most complexity-strewn an architecture, a most awe-inspiring bio-chemico-genetico-mechanism, that we humans will ever see in this Universe; nothing else will ever surpass this magnificence.
















And it all begins with the book of genome, that has already been written, that will have all the tools to keep on writing the future of a human physiology and with that begins the human life and soon the Cardiology is formed and follows neurology: the duo or the two in one or the one in two: for they, neither ends nor begins alone but, rather, both just clasp, grasp, sew, knit, cut, run, crisscross, bind, bend, blend and flow in, out, between and through the human physiology in such an 'infinity of subtle, intricate and sublime artistry', that the entire creation of this Universe does not have a parallel to show next to it. And with this Cardiology and Neurology the human becomes more than a physiology: it becomes a human mind and that has not been written out, unlike the genome, which has been, and, here is, where the entire life of this human mind is, as if it has got infinity of white papers bundled into a beautiful blank book, that no one can know how to write but that human mind alone does and this is where humanity is, this is what humanity is and this is how humanity is and this why we publish The Humanion to write a Beautiful Book out of those blank white pages of that book, where genome alone can never write a single word unless The Sanctum Mayakardium and The High Neuranium join forces to make 'one': the one, that is exactly like the heart with two atria; or the one, that is exactly like the brain with two hemispheres: it is two in one and one in two. And here is to this awe, to Humanity

New Method Developed for Studying ALS More Effectively



|| January 17: 2019: Karolinska Institutet News || ά. The neuro-degenerative disease ALS causes motor neuron death and paralysis. However, long before the cells die, they lose contact with the muscles as their axons atrophy. Researchers at Karolinska Institutet have now devised a new method, that, radically, improves the ability to study axons and, thus, to better understand the pathological development of ALS. The method is described in the scientific journal Stem Cell Reports. All neurons have a fibre-like projection, called, an axon and those of motor neurons can be extremely long, over a metre, as they have to stretch from the spinal cord to the muscles of the arms and legs.

It is known that in ALS the motor neurons die backwards and lose functionality where the axon meets the muscle before, gradually, atrophying completely. By examining the presence of RNA in a cell, it is possible to discover which genes are switched on and off and, thus, the cell’s function and general condition. In long-axoned neurons, there is a buffer of RNA in the axon, that enables them to, quickly, interact with their environment, e.g, muscle cells.

Scientists are keenly interested in investigating the repertoire of RNAs in motor axons of healthy individuals and ALS patients to gain deeper insight into disease processes. However, this has proven to be very difficult as the amount of RNA in axons is minute. If, just one single cell body gets into the axon study material, it will contaminate it with its own RNA, making it impossible to see what the axon’s RNA reservoir looks like.

“We have now developed a greatly improved method for this, called, Axon-seq.” says Associate Professor Eva Hedlund,  at the Department of Neuro-science, Karolinska Institutet. “It’s a relatively cheap, simple and highly sensitive method, that we’ve described in detail in our study so that it can be used by other researchers interested in studying neuronal processes.”

Her research group has used the method to examine motor neurons, generated from mouse and human stem cells. Their results show that the axon’s reservoir of RNAs differs, significantly, from that of the cell body, which is a new discovery. The researchers, also, examined the transcriptome of ALS-diseased motor neurons and found that in neurons with the mutated version of the SOD1 gene, that causes ALS, the axon’s RNA profile differed from that of healthy cells.

“Many of the genes we found dysregulated in ALS are needed for the normal function of the axon and its contact with the muscle.” says Mr Jik Nijssen, doctoral student and one of the authors the study with MR Julio Aguila Benitez. “Many of these genes present possible targets for future therapies.”

The study was financed by the Swedish Research Council, the EU Joint Programme,  Neuro-degenerative Disease Research:JPND, the Strategic Research Area in Neuroscience at Karolinska Institutet, the Birgit Backmark Endowment for ALS Research at Karolinska Institutet in memory of Nils and Hans Backmark, the Åhlén Foundation, the Ulla-Carin Lindquist Foundation for ALS Research, the Magnus Bergvall Foundation, the Swedish Society for Medical Research and the Swedish Brain Fund.

The Paper: Axon-seq decodes the motor axon transcriptome and its modulation in response to ALS: Jik Nijssen, Julio Aguila Benitez, Rein Hoogstraaten, Nigel Kee, Eva Hedlund: Stem Cell Reports: Online December 11: 2018:::ω.

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Brain Activity Shows the Development of Visual Sensitivity in Autism




|| December 17: 2018: University of York News|| ά. Research, investigating how the brain responds to visual patterns in people with Autism, has shown that sensory responses change between childhood and adulthood. The differences observed between adult and young people mimicked those seen in a strain of fruit flies, that had a genetic change associated with Autism and other developmental conditions. This demonstrates that sensory issues in Autism can be modelled in fruit flies, providing an opportunity to further understand the complexities of the condition.

Individuals with Autism, often, report sensitivity to bright lights and loud sounds, as well as, a variety of other sensory disturbances and differences. These can lead to problems in their everyday life, for example, they, might, avoid bright or noisy environments. Currently, however, there is limited research on the underlying mechanisms to explain why people with Autism experience discomfort during some sensory experiences. To investigate this, the researchers asked both children and adults, with and without Autism, to look at patterns on a computer screen, that flickered at specific rates.

The researchers, then, measured the way neurons in the participant’s brain responded to the flickering patterns using an electroencephalogram:EEG, which detects electrical activity in the brain. Dr Greta Vilidaite, who completed the study whilst doing her PhD at the University’s Department of Psychology, said, “Some neurons in the visual parts of the brain fired at the same frequency as the flickering patterns, at five times per second, for example, while other types of neurons responded at twice this frequency.

In adults with Autism and in our mature mutant flies, we found a reduction in brain activity at this higher frequency compared to control participants. In children and in juvenile flies, responses were lower at both frequencies. This suggests that sensory differences, may, change during development, perhaps, through some process of compensation or adjustment.”

The new findings, part of a collaboration between the University of York and Stanford University, helped scientists understand the link between the differences in brain activity in adults and children and a specific genetic change, associated with Autism, as modelled in fruit flies. 

The findings will allow future studies to understand the precise mechanisms, involved in how sensory perception is affected in Autism and whether the difference in brain responses between adults and children has any impact on how they perceive visual or other sensory stimuli.

Dr Chris Elliott, from the University of York’s Department of Biology, said, “We, now, have a clearer picture of one sensory difference and have a genetic fly model, that reflects this same difference.

It is possible that in future the fruit fly model could be used to test potential treatments to alleviate some of the sensory difficulties experienced by people with Autism.”:::ω.

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Idiopathic Intracranial Hypertension: New Guidelines Aim to Improve Diagnosis and Treatment of the Neurological Condition




|| October 17: 2018: University of Birmingham News || ά. Experts, led by the University of Birmingham, have produced the first internationally collaborative guidelines, aimed at improving the treatment and diagnosis of a rare condition, which causes devastating high brain pressure. Idiopathic Intracranial Hypertension, also, known as, IIH, is caused by high pressure in the brain with consequences from blindness to incapacitating daily long-term headaches. The condition, mainly, affects obese women in their 20s and 30s. Once regarded as rare, the disease incidence is now on the rise in line with the global rise in obesity.

There are very limited treatment options and practices vary widely around the UK and internationally and, up until now, there have been no previous guidelines for the management of the condition. Now, new guidelines have been created by a group of specialists in neurology, neuro-surgery, neuro-radiology, ophthalmology and neuro-radiology, who have had expertise in managing IIH. The patient charity IIHUK had an active role in contributing to the guideline development. The team envisage that the new guidelines, published in Journal of Neurology Neuro-surgery and Psychiatry, will revolutionise the treatment of the condition.

Extensive research was carried out to enable the creation of the guidelines, including, a survey of consultants, who investigate and manage IIH regularly, as well as, a comprehensive systemic literature review. Sufferers of the condition were, also, heavily involved in the process.

The guidelines were, also, reviewed prior to publication by a range of professional bodies, namely, the Association of British Neurologists:ABN, the Society of British Neurological Surgeons:SBNS, the Royal College of Ophthalmologists:RCO and the British Association for the Study of Headache:BASH.

Senior and Corresponding Author Dr Alex Sinclair, of the University of Birmingham’s Institute of Metabolism and Systems Research, said, “This guideline will have significant impact on patient care internationally. It is a vital step to standardise and ensure safe, high quality care for all patients.”

Lead Author Ms Susan Mollan, of the University of Birmingham’s Institute of Metabolism and Systems Research said, “The guideline has highlighted multiple areas of uncertainty in the management of IIH. They represent key areas for future research. As further research emerges the guidelines will be updated.”

Dr Alex Sinclair is, also, an Honorary Consultant Neurologist and Clinician Scientist at University Hospitals Birmingham NHS Foundation Trust. Dr Alex Sinclair is funded by a National Institute for Health Research:NIHR: Clinician Scientist Fellowship. 

The Paper: Idiopathic intracranial hypertension: consensus guidelines on management: Mollan et al 2018: Published: Journal of Neurology Neuro-surgery and Psychiatry. DOI: 10.1136/jnnp-2017-317440

About Idiopathic Intracranial Hypertension: Idiopathic Intracranial Hypertension is a rare condition, with an incidence in the general population of one per 100,000, rising to 20 per 100,000 in women, who are obese. IIH is caused by increased generation of cerebrospinal fluid and characterised by raised intracranial pressure, resulting in disabling daily headaches and optic disc swelling. A previous study by the University of Birmingham research team has shown that weight loss is successful in relieving IIH.

Caption: Dr Alex Sinclair: University of Birmingham’s Institute of Metabolism and Systems Research: Image: University of Birmingham:::ω.

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First Patient Trial Will Test New Approach to Treating Alzheimer’s Disease: Upto 100 Patients Being Recruited Now




|| October 10: 2018: UCL News || ά. The first clinical trial of a new approach to modifying the progression of Alzheimer's Disease has opened in London, led by UCL researchers. The study is being conducted at the National Institute for Health Research:NIHR University College London Hospitals:UCLH Clinical Research Facility at the Leonard Wolfson Experimental Neurology Centre at Queen Square, assisted by the Royal Free Hospital. The trial, called, DESPIAD, will test whether a drug, that removes a protein, called, serum amyloid P component, from the brain, is helpful for patients with Alzheimer’s Disease.

Alzheimer’s Disease is the most common cause of Dementia and symptoms include memory loss and difficulties with thinking, problem solving and language. Dementia affects more than 35 million people worldwide, a number, that is expected to almost double every 20 years as populations across the developed world age. Despite multi-billion dollar investments and the commissioning of many large scale clinical trials over the past 20 years, no effective treatments have yet emerged. “After a long struggle for funding of our different approach to possible treatment of Alzheimer’s Disease, it is exciting to, finally, have started the DESPIAD trial, which has been made possible by the NIHR and the Wolfson Foundation.  We now hope it can proceed as swiftly as possible.” said Professor Sir Mark Pepys, UCL Medicine, who led the development of the new drug.

Almost, all medications tested have been focussed on the abnormal fibrous protein accumulations, known as amyloid plaques and neurofibrillary tangles, which are always present in the brain in Alzheimer’s Disease. The drugs have aimed at removing or preventing the formation of these abnormal deposits. There is good evidence that the proteins forming the abnormal fibres are closely related to development of the disease but nobody actually knows for sure what directly causes the death and loss of brain cells, that leads to dementia.

The laboratory of Professor Pepys has been working on amyloid for more than 40 years. He and his team have focussed on a normal, non-fibrous protein, called, serum amyloid P component:SAP, which is always associated with amyloid fibres in the body. They have shown that SAP contributes to the formation of amyloid and its persistence in the tissues.

In addition, SAP itself, unrelated to its role in amyloid, damages brain cells. The brain in Alzheimer’s Disease contains more SAP than normal because of the binding of SAP to the plaques and tangles. It is, therefore, possible that SAP directly causes death of brain cells leading to dementia.

In order to target SAP and prevent its harmful effects, Professor Pepys, Director of the Wolfson Drug Discovery Unit at UCL’s Royal Free Campus, developed a drug, called, Miridesap, which removes SAP from the blood. Miridesap has been given to patients with various diseases over the past 18 years, with no significant adverse effects. Because SAP is not made in the brain, removing the protein from the blood with Miridesap, also, removes all the SAP from the brain and from the amyloid deposits in the brain.

The NIHR, via the NIHR Biomedical Research Centre at University College London Hospitals, has lately funded the essential clinical trial required to determine whether Miridesap treatment is helpful in patients with Alzheimer’s Disease.

The ‘Depletion of serum amyloid P component in Alzheimer’s Disease’ trial, known as, DESPIAD, is led by Professor Martin Rossor, UCL Queen Square Institute of Neurology, who is, also, the NIHR National Director for Dementia Research.

“We desperately need new drug targets for Alzheimer’s Disease and so this trial, which is a novel approach, needs to be completed as soon as possible.” said Professor Rossor.

DESPIAD is recruiting patients with mild Alzheimer’s Disease, who will each be treated for one year and tested for changes in brain structure and function. The trial will run for about three years. The study is active and open to recruitment but is limited to 100 participants.

This non-commercial trial is sponsored by UCL and entirely funded by the NIHR; manufacturing assistance is provided by GlaxoSmithKline.

For further information about the trial, contact the DESPIAD team at uclh.despiad atω.

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New Research Gains New Insight on How Neurons Communicate With Muscles



|| October 08: 2018: Karolinska Institutet News || ά. Researchers at Karolinska Institutet have discovered a new way, in which nerve cells can control movement. In a study on Zebrafish published in the journal Proceedings of the National Academy of Sciences, they show that the contact between neurons and muscles is more dynamic than previously thought. The results can open up new avenues to treating spinal cord injury and certain neurological diseases. 

The ability to move deliberately is essential to the survival of all animal life and is based on an interaction between the muscles and the brain. The site, where motor neurons and muscle cells communicate with each other is called the neuro-muscular junction. This is where the neurons transfer signal substances, that can be taken up by the muscle cells to make them contract. This point of contact, the synapse, has long been described as a relatively simple system in adult vertebrates, with the molecule acetylcholine as the most important neurotransmitter.  

Despite this, knowledge is lacking on how the communication is actually effected and how adult motor neurons can respond to damage or environmental change. Researchers have now generated new knowledge about how the neuromuscular junction works. Their results show that it is a more dynamic system than previously believed. 

“Our study shows that the function of the neuro-muscular synapses can change under certain conditions and in certain diseases in order to fine-tune movements, which was a completely unexpected finding.” says Assistant Professor Konstantinos Ampatzis at the Department of Neuroscience, Karolinska Institutet, who led the study. 

The study was conducted on Zebrafish, which is a common model system in neuro-biological research. The researchers show that changes in the form of an increase in physical activity and spinal damage can cause certain adult motor neurons to switch from producing acetylcholine to producing another neuro-transmitter, glutamate. The researchers believe that this is to control movements better. 

The results indicate that more detailed studies of the neuro-muscular junction are needed, not least, in humans. Such knowledge is important because impaired communication between neurons and muscles can cause serious diseases, such as, the neuro-muscular disease Myasthenia Gravis. 

“Our study can open new doors to the treatment of diseases involving reduced neuro-muscular transmission.” says Dr Ampatzis. “More detailed knowledge on which neurons express specific neuro-transmitters can enable the development of better treatments, that restore function to the nervous system.” 

There is, also, growing evidence that the neuro-muscular junction is involved in the early stages of such diseases as Spinal Muscular Atrophy:SMA and Amyotrophic Lateral Sclerosis:ALS, which have previously been regarded as diseases of the motor neurons. 

The study was financed by the Swedish Research Council, the Strategic Research Area Neuroscience, the Swedish Brain Foundation, the Längman Cultural Foundation and Erik and Edith Fernström Foundation. 

The Paper: Adult spinal motoneurons change their neurotransmitter phenotype to control locomotion: Maria Bertuzzi, Weipang Chang, Konstantinos Ampatzis: Proceedings of the National Academy of Sciences: Online: October 01: 2018

Caption: Konstantinos Ampatzis: Researcher: Department of Neuroscience: Karolinska Institutet: Image: Stefan Zimmerman:::ω.

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People with Fibromyalgia Have Inflammation of the Brain




|| September 27: 2018: Karolinska Institutet News || ά. The causes of the difficult to treat pain syndrome Fibromyalgia are largely unknown. Using PET brain imaging, researchers at Karolinska Institutet and Massachusetts General Hospital have now shown that glial cells, the central nervous system’s immune cells, are activated in the brains of patients with Fibromyalgia. The finding has been published in the scientific journal Brain, Behaviour, and Immunity and, these findings, may, open the way for new therapies.

Fibromyalgia is a chronic pain syndrome, that causes extensive pain in the muscles and joints, severe fatigue, insomnia and cognitive difficulties. The higher pain sensitivity, that is characteristic of the syndrome, has been related to functional and structural alterations of brain regions associated with pain processing. In 2012, Professor Eva Kosek’s research group at Karolinska Institutet showed that patients with Fibromyalgia had elevated levels of certain inflammatory substances, cytokines, in the cerebrospinal fluid, suggesting inflammation of the central nervous system.

Their findings were, subsequently, corroborated by other researchers but the source of the inflammation remained unknown. Using modern positron-emission topography:PET brain imaging Professor Eva Kosek’s team has now been able to show that the central nervous system’s immune cells, called, glial cells, are activated and, thus, give rise to inflammation of the brain.

“As far as we know, this is the first time it’s been shown that glial cells are involved in the pathogenesis of Fibromyalgia.” says Professor Eva Kosek from the Department of Clinical Neuroscience, Karolinska Institutet. The results show that in Swedish and American patients with Fibromyalgia, glial cells are activated in large parts of the cerebral cortex and that the degree of activation was related to the degree of fatigue reported by the patients.

“The findings, may, open the way for the development of completely new therapies for this currently difficult to treat condition.” says Professor Kosek. “The fact that scientific research is able to demonstrate objective aberrations in the brains of people with Fibromyalgia will, hopefully, mitigate the suspicion with which patients are, often, treated by the health services and society.”

Today, an estimated 200,000 Swedes, mainly, women, suffer from Fibromyalgia. The brains of people with the condition are known to have an impaired ability to dampen pain signals, which means that things that are, normally, painless, cause considerable discomfort. 

The study was a collaboration between Professor Eva Kosek’s research group at Karolinska Institutet in Sweden, the PET Centre at Karolinska Institutet and Dr Marco Loggia’s research group at Martinos Centre for Bio-medical Imaging at Massachusetts General Hospital, USA.

The research in Sweden was financed from several sources, including, the EU’s 7th Framework and Programme and a donation from the Lundblad Family. The Swedish part of the project was, also, funded by Stockholm County Council, the Swedish Research Council, the Swedish Rheumatism Association and the Swedish Fibromyalgia Association.

The Paper: Brain glial activation in fibromyalgia – A multi-site positron emission tomography investigation: Daniel S. Albrecht, Anton Forsberg, Angelica Sandström, Courtney Bergan, Diana Kadetoff, Ekaterina Protsenko, Jon Lampa, Yvonne C. Lee, Caroline Olgart Höglund, Ciprian Catana, Simon Cervenka, Oluwaseun Akeju, Mats Lekander, George Cohen, Christer Halldin, Norman Taylor, Minhae Kim, Jacob M. Hooker, Robert R. Edwards, Vitaly Napadow, Eva Kosek, Marco L. Loggia: Brain, Behaviour and Immunity Online: September 14: 2018:::ω.


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New Large Scale Study Finds Stroke Doubles the Risk of Developing Dementia



|| September 03: 2018: University of Exeter News || ά. People, who have had a stroke, are around twice as likely to develop dementia, according to the largest study of its kind ever conducted. The University of Exeter Medical School led the study, which analysed data on stroke and dementia risk from 03.2 million people across the world. The link between stroke and dementia persisted, even, after taking into account other dementia risk factors, such as, blood pressure, diabetes and cardiovascular disease.

These findings give the strongest evidence to date that having a stroke significantly increases the risk of dementia. The study builds on previous research, which had established the link between stroke and dementia, though, had not quantified the degree to which stroke, actually, increased dementia risk. To better understand the link between the two, researchers analysed 36 studies, where participants had a history of stroke, totalling data from 01.9 million people. In addition, they analysed a further 12 studies, that looked at whether participants had a recent stroke over the study period, adding a further 01.3 million people.

The new research, published in the leading dementia journal Alzheimer's and Dementia: The Journal of the Alzheimer's Association, is the first meta-analysis in the area. Dr Ilianna Lourida, of the University of Exeter Medical School, said, “We found that a history of stroke increases dementia risk by around 70% and recent strokes more than doubled the risk. Given how common both stroke and dementia are, this strong link is an important finding. Improvements in stroke prevention and post-stroke care, may, therefore, play a key role in dementia prevention.”

According to the World Health Organisation, 15 million people have a stroke each year. Meanwhile, around 50 million people globally have dementia, a number expected to, almost, double ever 20 years, reaching 131 million by 2050. Stroke characteristics, such as, the location and extent of brain damage, may, help to explain variation in dementia risk observed between studies and there was some suggestion that dementia risk, may, be higher for men following stroke.

Further research is required to clarify whether factors, such as, ethnicity and education modify dementia risk following stroke. Most people, who have a stroke do not go on to develop dementia, so further research is, also, needed to establish whether differences in post-stroke care and lifestyle can reduce the risk of dementia further. 

Dr David Llewellyn, from the University of Exeter Medical School, said, “Around a third of dementia cases are thought to be potentially preventable, though, this estimate does not take into account the risk associated with stroke. Our findings indicate that this figure could be, even, higher and reinforce the importance of protecting the blood supply to the brain, when attempting to reduce the global burden of dementia.”

The research was supported by the Mary Kinross Charitable Trust, the Halpin Trust, the National Institute for Health Research:NIHR Collaboration for Leadership in Applied Health Research and Care for the South West Peninsula and the National Institute on Aging:NIA:National Institutes of Health:NIH.

The Paper: Stroke and dementia risk: A systematic review and meta-analysis: Published in Alzheimer’s and Dementia: Elżbieta Kuźma, Ilianna Lourida, Sarah F. Moore, Deborah A. Levine, Obioha C. Ukoumunne, and David J. Llewellyn:::ω.

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The New Detailed Atlas of the Nervous System of a Mouse




|| August 15: 2018: Karolinska Institutet News || ά. Researchers at Karolinska Institutet have created a systematic and detailed map of the cell types of the nervous system of mouse. The map, which can provide new clues about the origin of neurological diseases, is presented in the journal Cell. The researchers will now use the same methods to map out the human brain on a detailed level. The nervous system consists of hundreds, perhaps thousands, of different neurons but, also, immune cells, supporting glia cells and cells, that constitute vessels and membranes.

Our knowledge of these cell types mainly stems from microscopy, which provides information about the shape of cells and can detect certain proteins and from electro-physiology, where cells are distinguished based on their electrical properties. However, these methods are limited and there is currently no systematic atlas of the various cell types, that make up the mammalian nervous system. In recent years, Professor Sten Linnarson’s research group and others, have developed methods to map cell types of the brain more systematically in much greater detail than ever before, by measuring gene activity in individual cells.

“You can compare it to the difference between a medieval map and a satellite image: thousands of details, that were previously invisible become visible with the use of these new techniques and the entire map becomes more reliable.’’ says Professor Sten Linnarson at the Department of Medical Biochemistry and Biophysics at Karolinska Institute.

His research group now publishes the largest study of the architecture and composition of the mammalian nervous system to date, using the mouse as a model system. The researchers identified 265 different types of cells and found that neurons had the greatest diversity with over 200 different types.

"What surprised us most was that we discovered several different types of astrocytes, that were specialised in different parts of the brain. This suggests that astrocytes have specific functions in different parts of the brain and that they play more of a key role in the functions of the brain than previously understood." says Professor Sten Linnarson.

The knowledge of the cell types of the brain can be used to understand the origin of different diseases. Roughly, one third of all neurological diseases arise during embryonic development. In the past fifteen years a large number of genetic studies have identified the genes, that contribute to diseases, such as, Schizophrenia, Multiple Sclerosis, Autism, Alzheimer’s and Parkinson’s Disease.

However, diseases originate from a specific type of cells, in a specific location and at a specific time depending on where and when the relevant genes are active. "With the help of our new atlas of the nervous system, researchers are now able to place disease-causing genes in specific cell types, which provides us with clues as to how the disease occurs. In the long run, this, might, contribute to the development of new drugs or other therapies.", says Professor Linnarson.

The mapping of the mouse nervous system is an important first step in a larger project, where researchers are now mapping the human brain by using the same methods. The current study was funded by the Knut and Alice Wallenberg Foundation, the Swedish Foundation for Strategic Research and the Wellcome Trust.

The Paper: Molecular Architecture of the Mouse Nervous System: Amit Zeisel, Hannah Hochgerner, Peter Lönnerberg, Anna Johnsson, Fatima Memic, Job van der Zwan, Martin Häring, Emelie Braun, Lars Borm, Gioele La Manno, Simone Codeluppi, Alessandro Furlan, Kawai Lee, Nathan Skene, Kenneth D. Harris, Jens Hjerling Leffler, Ernest Arenas, Patrik Ernfors, Ulrika Marklund, Sten Linnarsson: Cell: Online August 09: 2018:::ω.

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Charcot-Marie-Tooth: A Genetic and Neurological Disorder: Charcot-Marie-Tooth UK Is Seeking to Raise Awareness of the Condition Throughout September



|| August 13: 2018 || ά. This little-known neurological condition can cause balance problems and falls, pain, fatigue and deformities in hands, lower legs and feet and it is called Charcot-Marie-Tooth Disorder or CMT. Throughout September, Charcot-Marie-Tooth UK, a charity, raising awareness of this genetic, neurological disorder, that can cause uncontrollable pain, chronic fatigue and deformities in the hands, lower legs and feet, leading to balance problems and falls, will be seeking to raise awareness of this condition.

Professor Mary Reilly, of Clinical Neurology and Consultant Neurologist at UCLH, also, Patron of Charcot-Marie-Tooth UK.  She says, “CMT has many different characteristics but, commonly, there is weakening and loss of muscle and reduced sensation, predominantly, in the feet and legs but, also, in the hands and arms in the advanced stages of disease. These lead to a range of orthopaedic complications, leading to a variety of mobility and dexterity problems and sometimes scoliosis.

CMT does not describe a single disorder but a group of conditions. It is important to determine exactly what kind of CMT someone has, in order to improve their quality of life and this can, only, be done once a diagnosis is considered in a patient. Anecdotal evidence from CMT UK tells us this takes much longer than we would like and many people put up with CMT for a long time thinking they are clumsy or have funny feet, suffering in silence, when they could be receiving help and support.

As a professor of Clinical Neurology, whose main clinical and research interest is inherited neuropathies like CMT, I have first-hand experience of how useful and critical the input from Charcot-Marie-Tooth UK is to this patient community. The charity provides an excellent information resource for patients and everyone we see in the clinic we give its details to access its literature, website resources and online discussion forums.”

CMT Awareness Month is being launched by on Saturday, September 01. Last year, the campaign received an unexpected boost, when former Girls Aloud star, Ms Cheryl Tweedy, joined in to raise awareness of the condition, through speaking about the affects this condition had had on her friend’s son. A leading neurological specialist, Professor Mary Reilly estimates around 23,000 people in the UK have Charcot-Marie-Tooth, which is named after the three scientists, who discovered it. Steadily progressive, the condition causes muscle weakness and wasting in the lower legs and feet, leading to problems like hammer toes, restricted mobility, and uncontrollable pain. 

The hands and fingers are affected, making tasks needing fine motor skills, such as, fastening shoe laces and buttons, very difficult.  Although, CMT is not life-threatening, for many, it will impact on and significantly reduce the quality of their lives, with some people, even, ending up as wheelchair users.

This year’s campaign aims to raise awareness of the symptoms of CMT among people, who have the condition but have not yet been diagnosed; make more medical professionals aware of the condition so people, who have CMT can get diagnosed and seek help; let people, who have CMT know that the charity exists and is there to offer advice and support and to raise funds to help Charcot-Marie-Tooth UK members and pay for vital research into the condition.

CMT UK’s Chief Operating Officer, Ms Karen Butcher can trace the CMT back six generations in her family.  She said, “There are still too many medical professionals, including, GPs, physiotherapists, orthotists, surgeons and, even, neurologists, that still don’t know what CMT is. Therefore, an integral part of this year’s campaign will be to educate them about the condition so they can help make a diagnosis, if, needed.

It is, also, important for us to reach those people, who think they might have the condition but haven’t been diagnosed yet.  Sometimes the symptoms aren’t obvious but due to the fact that CMT affects the hands and feet, it could be, they have trouble balancing, find they regularly trip or fall over and are constantly tired.  For some women, a telling sign is that they can’t wear high heel shoes due to high arches and hammer toes. 

There could be many reason for symptoms like these but, if, you have any, it would be a good idea to ask your GP about CMT. Early diagnosis helps improve the lives of those with the condition and because there’s a 50% chance it can be passed on from a parent to a child, professional genetic counselling can, also, be given.

We know it’s an ambitious strategy but, ideally, we’d like every new person told they have CMT to be automatically referred to us at the point of diagnosis so we can offer our support with benefits, jobs and family issues and advise them on where to get specialist medical help.”

Charcot-Marie-Tooth UK offers advice on how to manage the condition, as well as, support with benefits, jobs and family issues.  It says that while CMT is currently incurable, it can be managed effectively, so the right referrals to the right clinicians are crucial to improve the lives of those with the condition and proper genetic counselling should be received so the risks to the next generation can be learned.

To learn more about CMT visit the website of the charity or contact 0300 323 6316 or, to donate by visiting.

Professor Mary Reilly MD FRCP FRCPI is Professor of Clinical Neurology and Consultant Neurologist; President Association of British Neurologists, Head of Division of Clinical Neurology, Institute of Neurology, MRC Centre for Neuromuscular Diseases National Hospital for Neurology and Neurosurgery and UCL Institute of Neurology.:::ω.

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Sleep Disturbances Found to Have Been Linked to Increased Dementia Risk




|| July 29: 2018: Karolinska Institutet News || ά. Researchers at Karolinska Institutet in Sweden report that sleep disturbances in midlife or in late life are associated with a higher risk for developing Dementia in old age. The results are published in Alzheimer’s and Dementia: The Journal of the Alzheimer's Association. The results show that in midlife, when participants were in their 40s or 50s, insomnia was associated with a 24 per cent increased risk for Dementia later in life.

In late life, when participants were in their 60s or 70s, terminal insomnia, waking up too early, was associated with a doubled risk for later Dementia, while long sleep duration, more than nine hours of sleep per night, was associated with a four-fold increased risk for later Dementia. The latter finding among this older population, may be, due to already existing undiagnosed Dementia-related pathology, as dementia is, often, linked with sleep disturbances, including, increased sleep duration.

“Our findings have direct clinical implications and combined with previous studies they indicate that different stages in the life course are sensitive to sleep disturbances, which, in turn. increase the risk for Dementia. These sleep disturbances necessitate closer clinical attention and the implementation of tailored interventions.” says the Lead Author Dr Shireen Sindi, Post-Doctoral Researcher at Karolinska Institutet’s Department of Neurobiology,

The analysis included three population-based studies from Sweden and Finland with large sample sizes of men and women, more than 2,000, long follow-up durations, assessment of multiple sleep parameters and standardised Dementia diagnoses, adjusting for potential influencing factors, such as, levels of physical activity, genetics and sleep medications.

Dr Sindi works within the Nordic Brain Network team, led by Professor Miia Kivipelto  at Karolinska Institutet, focusing on lifestyle interventions for Dementia. They published the landmark Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability:Finger trial, which showed that a ‘multi-domain intervention’, including, diet, exercise, cognitive training and management of vascular risk factors, has a positive impact on cognitive functioning. More recently, many countries are adapting the Finger model to their local settings, e.g,  USA, China, Singapore, Canada, within the World-Wide Fingers platform. 

“It is promising that lifestyle changes can positively impact cognition. So far, there has been insufficient evidence regarding the role of sleep disturbances as a risk factor for Dementia. Our current study indicates that future interventions to prevent Dementia, may, benefit from, also, including, interventions to improve sleep.” says Dr Sindi.

The research team will now continue investigating the association between sleep disturbances and cognitive performance and Dementia among different populations, including, memory clinic patients. They will, also, examine the role of underlying biological mechanisms.

The study was done in collaboration with researchers at Karolinska Institutet’s Aging Research Centre Sweden, Centre for Ageing and Health, University of Gothenburg, Sweden, the National Institute for Health and Welfare in Helsinki, Finland, the University of Eastern Finland and Stockholm University: Stress Research Institute, Sweden.

The research was financed by Alzheimerfonden, the Swedish Research Council, the Swedish. Research Council for Health, Working Life and Welfare, Cimed, Karolinska Institutet, Le Fonds de recherche du Québec; Santé, Konung Gustaf V:s och Drottning Victorias Frimurarestiftelse, the Knut and Alice Wallenberg Foundation, the Swedish Brain Foundation, and Swedish Brain Power.

The Paper: Sleep disturbances and dementia risk: a multi-centre study: Shireen Sindi, Ingemar Kåreholt, Lena Johansson, Johan Skoog, Linnea Sjöberg, Hui-Xin Wang, Boo Johansson, Laura Fratiglioni, Hilkka Soininen, Alina Solomon, Ingmar Skoog, and Miia Kivipelto: Alzheimer’s and Dementia: The Journal of the Alzheimer's Association, online 17 July 2018, doi: 10.1016/j.jalz.2018.05.012:::ω.

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Exposure to Solvents and Smoking are Linked to Increased Risk to Develop Multiple Sclerosis

|| July 08: 2018: Karolinska Institutet News || ά. People, who carry the genes, that make them more susceptible to developing Multiple Sclerosis:MS are at much greater risk of developing the disease, if, they have been exposed to paint, varnish and other solvents, according to a new study from Karolinska Institutet published in the journal Neurology. If, they have, also, been smokers, the risk of developing MS is increased.

The study shows that people, who have been exposed to paint or other solvents are 50 per cent more likely to develop MS than people with no exposure. People with exposure to solvents, who, also, carry certain gene variants, that make them more susceptible to MS are ten times as likely to develop the disease as people with no solvent exposure, who do not carry the MS genes.

People with exposure to solvents, who carry the MS genes and, in addition to that, have been smokers are as much as 30 times more likely to develop MS, compared to those,  who have never smoked or been exposed to solvents and who do not have the genetic risk factors. How these different factors interact to create a much greater risk than they do on their own is not yet known.

”It’s possible that exposure to solvents and smoking, may, both involve lung inflammation and irritation, that leads to an immune reaction in the lungs.” says the Lead Author Dr Anna Karin Hedström at the Institute of Environmental Medicine and the Department of Clinical Neuroscience, Karolinska Institutet.

“How this cocktail of MS genes, organic solvents and smoking contributes so significantly to MS risk warrants investigation.’’  says Dr Gabriele C. DeLuca, MD, PhD, of the University of Oxford in the United Kingdom, in an accompanying editorial.

“In the meantime, avoiding cigarette smoke and unnecessary exposure to organic solvents, particularly, in combination with each other, would seem reasonable lifestyle changes people can take to reduce the risk of MS, especially, in people with a family history of the disease.”

The study included more than 2,000 people, who had recently been diagnosed with MS in Sweden and, almost, 3,000 people of the same age and sex without MS. Blood tests were used to determine which human leukocyte antigen gene variants the participants had.

They were, also, asked about previous exposure to organic solvents, painting products or varnish and whether they had ever been a smoker. One limitation of the study is that it is possible that the participants, may not, have remembered correctly. Moreover, since it is an observational study no definitive conclusions can be drawn regarding causality.

The study was funded by the Swedish Research Council, Swedish Research Council for Health, Working Life and Welfare, Knut and Alice Wallenberg Foundation, AFA Insurance, Swedish Brain Foundation and Neuro Sweden.

The Paper: Organic solvents and MS susceptibility; interaction with MS risk HLA genes: Anna Karin Hedström, Ola Hössjer, Michail Katsoulis, Ingrid Kockum, Tomas Olsson, Lars Alfredsson: Neurology: Online: July 03: 2018 

Caption: Anna Karin Hedström. Photo: Jannis Politidis:::ω.

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For Stories Published in Neurology in ||April || May || June || Neurology Arkive 2018 Q-Beta


|| April 06: 2018 || ά. The Humanion was first published on September 24, 2015 and has been run, since that day, on a complete voluntary basis without any 'formal' or 'constituted' manner or form and, it was run on as a Human Enterprise, which is an idea of Humanics, in which, ownership is replaced by belongingship and, thus, in a Humanical Society, no one owns anything but everyone belongs to the whole as the whole belongs to everyone lawfully and equally and, it neither believes in nor makes money but human utilities, needs, aspirations, creativity, imagination and dreams are served without money, where everyone works and creates for all others as all others create and work for all others, thus, bringing in meaning and purpose to life along with it come natural justice, equality and liberty, that establish a true civilisation within the Rule of Law. And in one word, this system of human affairs management is called, Humanics and a society that runs itself in humanics is called a humanical society. Today, we have begun the process of 'constituting' this Human Enterprise, which does not exist in the current system, but the next closest thing to it, that exists in the UK Law is Social Enterprise. Therefore, today, Friday, April 06, 2018, we are beginning Regine Humanics Foundation, that is the 'Agency', that will lead, run, manage and develop everything, that The Humanion has been trying to do.

Regine Humanics Foundation is established by the Thinker, Author, Poet, Novelist, Playwright, Editor of The Humanion, Festival Director of London Poetry Festival and a Humanicsxian: hu: maa: neek: tian: One, that believes in, lives and exists by Humanics, Mr Munayem Mayenin, of London, England, United Kingdom. Mr Mayenin says, ''Humanics is a vision; people, may, call it, utopia, we, call it our Humanicsovicsopia; Humanics. Humanics is our philosophy, our faith, our conviction, our resolution, our way of existing, thinking, being and doing: to seek and try to do so in the determination that all we must do and be is to exist to advance the human condition. People, readers and agencies and organisations, from all across England, Scotland, Northern Ireland, Wales and the whole of the United Kingdom and Australasia, Africa, Asia, Europe, North and South America, from all walks and strata of life, have supported our endeavours, supported The Humanion and The Humanion Team, who volunteered their time to run things, since the beginning of The Humanion and long before that, when other things, that are now part of The Foundation, were developing. Nothing has changed in terms of the nature and value of what we have been seeking to do.''

''But the founding of The Foundation brings it all in a solid foundation so that we can keep on building this 'vision' so that it keeps on going regardless of who come to take the vision-mission of The Foundation forward. The Foundation runs along with time and along with the flowing humanity. This is the dream, this is the vision, this the hope in founding this Foundation. And, in this, we hope and invite all our readers, supporters, well wishers and all agencies and organisations to support our endeavours to build something, a Human Enterprise, which we are in the process of registering as a Social Enterprise, as a Community Interest Company, working for the common good of the one and common humanity. No one makes or takes profit out of The Foundation, which now runs The Humanion and everything else, that is part of it. The Foundation, once registered, will have an Asset Lock, which means that in any event, should The Foundation dissolve itself, all its existing assets shall go to a similar Social Enterprise. Therefore, we invite everyone to support The Foundation, support The Humanion in whatever way they can. And, there are endless number of ways people and organisations can support The Foundation and The Humanion.''::: ω.

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|| All copyrights @ The Humanion: London: England: United Kingdom || Contact: The Humanion: editor at || Regine Humanics Foundation Ltd: reginehumanics at || Editor: Munayem Mayenin || First Published: September 24: 2015 ||
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