Researchers discover new biological mechanism to regenerate and repair myelin

 

A study led by Dr. Hyun Kyoung Lee, associate professor at Baylor College of Medicine and investigator at the Jan and Dan Duncan Neurological Research Institute at Texas Children's Hospital, has discovered a new biological mechanism to regenerate and repair myelin, a protective sheath that insulates neuronal fibers and plays a vital role in ensuring rapid and accurate neurotransmission. The Duncan NRI team found novel roles for the Dishevelled associated activator of morphogenesis 2 (Daam2) protein and CK2α kinase in regulating myelin repair and regeneration. The study was published in the Proceedings of the National Academy of Science.

Myelin is produced by a type of glial precursor cells called oligodendrocytes (OLs) which are among the most numerous cells in the nervous system. Damage or loss of myelin sheath is the hallmark of various neurological diseases in adults (e.g. multiple sclerosis) and infants (e.g. cerebral palsy) and is common after brain injuries.

The Wingless (Wnt) signaling pathway is one of the key regulators of OL development and myelin regeneration. In certain diseased conditions and brain injury, its levels are elevated in the white matter, which impairs myelin production by forcing oligodendroctyes to remain in a "stalled/quiescent state".

A few years back, Dr. Lee and others found that a glial protein, Daam2 inhibits the differentiation of oligodendrocytes during development as well as myelin regeneration and repair. However, until now precise mechanisms underlying this process have remained a mystery.

To understand how Daam2 inhibits myelination, the team first needed to determine the regulation of Daam2 itself. Using biochemical approaches, they found two amino acid residues (Ser704 and Thr705) of Daam2 protein undergo phosphorylation - a common post-translational regulatory mechanism that turns on or off the activity of the proteins.

To explore if Daam2 phosphorylation affected the progression of OL lineage, they analyzed differentially expressed genes (DEGs) in wild-type and mutant animals whose Daam2 is constitutively phosphorylated. DEGs downregulated in the mutant OLs were enriched in genes involved in lipid/cholesterol metabolism whereas DEGs upregulated in the mutant OLs were involved in multiple signaling processes, including the Wnt pathway.

Since Daam2 is a known positive modulator of canonical Wnt signaling, they examined whether these DEGs were due to perturbations in Wnt signaling. They undertook a thorough developmental stage-specific analysis which revealed dynamic changes in the machinery and function of Wnt/β-catenin signaling in early versus late stages of OL development, and established that this signaling pathway is affected by Daam2 phosphorylation.

To identify the kinase(s) responsible for Daam2 phosphorylation, they conducted a motif analysis which found CK2, a Wnt/β-catenin signaling Ser/Thr kinase that was also one of the candidates in their biochemical and genetic screen. They further confirmed that its catalytic subunit, CK2α, interacted with Daam2 in lab-cultured OLs and also phosphorylated it. Moreover, both Daam2 and CK2α were sequentially upregulated in a manner that was concomitant with the progression of OL lineage. Using in vitro cultured OLs and in vivo mouse models, they found compelling evidence suggesting that CK2α promotes OL differentiation by phosphorylating Daam2.

Further studies using an animal model of neonatal hypoxic injury model revealed a beneficial role for CK2α-mediated Daam2 phosphorylation. They found that it plays a protective role in developmental and behavioral recovery after neonatal hypoxia, a form of brain injury seen in cerebral palsy and other conditions, and additionally, it facilitates remyelination after white matter injury in adult animals.

Together, these findings have identified a novel regulatory node in the Wnt pathway that regulates stage-specific oligodendrocyte development and offers insights into a new biological mechanism to regenerate myelin.

"This study opens exciting therapeutic avenues we could develop in the future to repair and restore myelin, which has the potential to alleviate and treat several neurological that are currently untreatable," Dr. Lee said.

The first author, Chih-Yen Wang is now an assistant professor in the National Cheng Kung University. Others involved in the study were Zhongyuan Zuo, Juyeon Jo, Kyoung In Kim, Christine Madamba, Qi Ye, Sung Yun Jung and Hugo J. Bellen. They are affiliated with one or more of the following institutions: Baylor College of Medicine and Jan and Dan Duncan Neurological Research Institute at Texas Children's Hospital. This work was supported by grants from NIH/NINDS, the National Multiple Sclerosis Society, the Cynthia and Anthony G. Petrello Endowment, and the Mark A. Wallace Endowment, the Eunice Kennedy Shriver National Institute of Child Health & Human Development of the National Institutes of Health for the BCM IDDRC Neurobehavior and Neurovisualization Cores. GERM core at Baylor College of Medicine helped with mouse line generation, scRNA-sequencing was partially supported by the SCG core and GARP core.

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Amygdala Hijack: When Emotion Takes Over

 

The amygdala is part of the limbic system, which regulates emotional and behavioral responses. An amygdala hijack is a fight-or-flight response to stress.

To better understand what an amygdala hijack is, you’ll need to understand a bit about how the brain functions. You’ll also need to understand two specific parts of the brain: the amygdala and the frontal lobes.

Fight or flight

The amygdalae are clusters of almond-shaped cells located in the brain’s base. Everyone has two in each hemisphere. They defineTrusted Source and regulate emotions, store memories, and attach those memories to specific emotions.

The amygdala also activates the fight-or-flight response. This response can help people in immediate physical danger react quickly for their safety and security. For example, the fight-or-flight response helped early humans respond to threats to avoid injury or death.

The amygdala activates this fight-or-flight response without any initiative from you. When that part of your brain senses danger, it signals your brain to pump stress hormones, preparing your body to either fight for survival or to flee to safety.

Today, that fight-or-flight response is more likely to be triggered by emotions such as stress, fear, anxiety, aggression, and anger.

 

 

Frontal lobes

To understand what an amygdala hijack is, you need to know about a second part of the brain: the frontal lobes. These two, large areas are located at the front of your brain.

The front lobes are part of the brain’s cerebral cortex. This area of the brain regulatesTrusted Source voluntary actions like reasoning, thinking, movement, decision-making, and planning. It is more rational than the amygdala.

The front lobes allow you to evaluate your emotions and then use your experiences and judgement to consciously respond. These reactions are not automatic, like the ones generated by the amygdala.

In the event of a physical threat, the amygdala may jump to the fight-or-flight response, but the front lobes process the information you’re receiving to help you determine if the danger is real. If the danger isn’t immediate, the frontal lobes help you decide what to do in response to the stress.

For mild or moderate threats, the frontal lobes can often override your amygdala so you can approach the situation rationally. But in the case of strong threats, the amygdala may trigger the fight-or-flight response.

For early humans, the fight-or-flight response was vital. The threat of physical harm was very real.

Today, however, you’re more likely to experience psychological threats, such as the pressures and stress of modern life, work, and relationships. These emotions, too, can trigger the amygdala’s fight-or-flight response.

Anger, aggression, fear, and stress are all common emotional triggers. They can cause sudden, illogical, and even irrational reactions.

In his 1995 book “Emotional Intelligence: Why It Can Matter More Than IQ,” psychologist Daniel Goleman named this emotional overreaction to stress “amygdala hijack.” The amygdala hijack occurs when your amygdala responds to stress and disables your frontal lobes. That activates the fight-or-flight response and disables rational, reasoned responses. In other words, the amygdala “hijacks” control of your brain and your responses.

 

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What Are Glial Cells and What Do They Do?

Glial cells are a type of cell that provides physical and chemical support to neurons and maintain their environment. Located in the central nervous system and peripheral nervous system, glial cells are sometimes called the "glue" of the nervous system, as well as neuroglia or just glia.

This article will go over what glial cells do in the brain and nerves in the body. You'll also learn about conditions that are related to glial cells.

 

Types of Glial Cells

Glial cells' main job is to support another type of brain cell called neurons. Glial cells are like a secretarial pool for your nervous system and its janitorial and maintenance staff.

Glial cells may not do the "big jobs," in the brain, but without them, those big jobs would never get done.

There are different types of glial cells and each one has a specific role in helping your central nervous system (CNS)—which is made up of your brain and the nerves of your spinal column—work right.

There are five types of glial cells in your CNS: Astrocytes

• Oligodendrocytes
• Microglia
• Ependymal
• cells
• Radial glia1

You also have glial cells in your peripheral nervous system(PNS), which is made up of all the nerves in your body that are away from your spine (like your arms and legs).

The two types of glial cells in the PNS are:

•  Schwann cells
• Satellite cells

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I have cerebral palsy and ran 10k in less than an hour

 

A Glasgow woman with cerebral palsy has completed a 10k run in less than an hour using a specially-adapted walking frame.

Just six years after an accident left her in chronic pain and using a wheelchair, she completed the Paisley race in 57 minutes.

Unable to walk unaided, Dr Julie McElroy used a frame runner - a cross between a tricycle and a walking frame.

The custom-made contraption has a saddle and body support, but no pedals.

"When I was on the road and when I was going downhill and on to the high street I really got such a buzz. The crowd were electrifying," she told BBC Radio Scotland's Drivetime with John Beattie

"By doing frame running in the Paisley 10k, it was about promoting inclusion. I wanted to show that I was able to take part in mainstream events alongside my peers.

"I just love having that independence of my frame to be able to run alongside all these fellow runners who do it day in, day out."

She was born with cerebral palsy (CP), a condition affecting her mobility, speech and hearing and she wears two hearing aids.

But she has not let it stand in her way, having completed a series of higher education qualifications, including a PhD.

The 37-year-old has also always enjoyed outdoor pursuits having previously climbed Ben Nevis, competed in Tall Ships excursions, the Kiltwalk and holding gold and diamond Duke of Edinburgh awards.

But a traumatic accident six years years ago left her in chronic pain and apprehensive about taking on the new challenge of frame running.

• What is Frame Running?
• How I drive with cerebral palsy
• From additional needs school to a PHD - Julie's story

She said: "I actually tore the groin muscle off my pelvis. I was in chronic pain, an excruciating burning pain. Nobody actually believed me.

"When you've got an underlying disability people just assume 'oh it's just a deterioration of your CP'.

"After a lot of investigations people finally believed me and I started to really think about what I wanted to do to get myself back out there."

She found support in the form of Gordon Innes, a coach at Victoria Park athletics club in Glasgow who specialised in working with athletes with disabilities.

"I could barely barely run two metres. I was just exhausted because I hadn't been actively involved in sports because of the injury.

"But Gordon took me under his wing and said 'I see a lot of potential, I'm willing to train you up'.

"I wouldn't be here if it wasn't for him and the way that he's nurtured me in the last two years and mastered my drive and motivation for frame running into road running events."

With encouragement from her coach, Julie decided to get fitted for a custom-made running frame which would support her daily training and build up the strength in her left leg following her accident.

She said: "At the time, I wasn't convinced I was making the right decision. The cost was astronomical. It came to a bill of £3,500.

"But for me personally its been worth the financial investment. Not only for my physical health and my mental health but look how far I've come in two years to getting myself back out there doing something different."

She is now working towards a half marathon (13.1 miles, 21 km) in October.

Her coach, Gordon, said: "Julie has never allowed her cerebral palsy to hold her back and since her accident she's even overcome the difficulties of running with an irreparable groin tear.

"She trains in all weathers without complaint and truly is an inspiration to everyone around her.

"She's enjoying the process of gradually moving from training and competing on the track to longer distances on the roads. I don't think anyone would bet against her succeeding."

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Electroencephalogram (EEG)

An electroencephalogram (EEG) is a test that measures electrical activity in the brain using small, metal discs (electrodes) attached to the scalp. Brain cells communicate via electrical impulses and are active all the time, even during asleep. This activity shows up as wavy lines on an EEG recording.

An EEG is one of the main diagnostic tests for epilepsy. An EEG can also play a role in diagnosing other brain disorders.

Why it's done

An EEG can find changes in brain activity that might be useful in diagnosing brain disorders, especially epilepsy or another seizure disorder. An EEG might also be helpful for diagnosing or treating:

Brain tumors
Brain damage from head injury
Brain dysfunction that can have a variety of causes (encephalopathy)
Sleep disorders
Inflammation of the brain (herpes encephalitis)
Stroke
Sleep disorders
Creutzfeldt-Jakob disease

An EEG might also be used to confirm brain death in someone in a persistent coma. A continuous EEG is used to help find the right level of anesthesia for someone in a medically induced coma.

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Nurse-Delivered Sleep Restriction Therapy Reduced Insomnia Symptoms

 

Sleep restriction therapy -- systematically restricting and regularizing time in bed to stabilize sleep -- conducted by a nurse in a primary care setting reduced insomnia symptoms compared with sleep hygiene alone, according to the randomized HABIT trial.

At 6 months, the mean score on the Insomnia Severity Index (ISI) was 10.9 among participants who received nurse-delivered sleep restriction therapy versus 13.9 for those who received a sleep hygiene booklet only (P<0.0001), reported Simon Kyle, PhD, of the Sleep and Circadian Neuroscience Institute at the University of Oxford in England,

Mean adjusted differences in ISI -- which ranges from 0 to 28, with higher scores indicating more severe symptoms -- also significantly favored the intervention at both 3 and 12 months as well:

• 3 months: -3.88 (95% CI -4.66 to -3.10, P<0.0001)
• 12 months: -2.96 (95% CI -3.75 to -2.16, P<0.0001)

In addition, the incremental cost per quality-adjusted life-year (QALY) gained was £2,076 ($2638) with sleep restriction therapy, suggesting that the treatment had a 95.3% probability of being cost-effective based on a £20,000 ($25,412) cost-effectiveness threshold, Kyle and team said.

"Insomnia is a serious condition because it's highly prevalent, has a major effect on quality of life, and increases risk for developing other physical and mental health problems," Kyle said in a statementopens in a new tab or window. "The key issue is that people with chronic insomnia rarely receive evidence-based treatment."

Guidelines suggest that first-line treatment for insomnia should be multi-component cognitive behavioral therapy, "but access is extremely limited worldwide because of inadequate resources and expertise," the authors noted, with patients instead often prescribed hypnotic medication or off-label sedative antidepressants.

Sleep restriction therapy is a principal component of cognitive behavioral therapy, which "counters behaviors that perpetuate insomnia, specifically time-in-bed extension, variability in sleep-wake timing, and daytime napping," Kyle and team explained.

This brief nurse-delivered therapy can be both effective in treating insomnia disorder and improving certain aspects of mental health and functioning for these patients, they pointed out, adding that their study results could have implications for clinical practice in primary care settings because it is cost-effective without major increases in demands on nursing time.

"Future research is needed to understand how the nurse-delivered program could be implemented in the NHS, for example as part of a stepped care approach to insomnia management, and whether this may lead to reduction in prescriptions for sleep medication," Kyle said.

In an accompanying commentaryopens in a new tab or window, Annemieke van Straten, PhD, of Vrije Universiteit Amsterdam in the Netherlands, and co-authors, agreed that this approach could become an important therapy option for patients with insomnia.

 

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"Neurodegenerative Diseases: Axonal Dysfunction and Therapeutic Approaches"

 

An axon is a long, slender projection of a nerve cell (neuron) that conducts electrical impulses away from the neuron's cell body. Axons are a fundamental part of the nervous system and play a crucial role in transmitting information within the brain, spinal cord, and throughout the body.

Here are some key points about axons:

1. Structure: Axons are typically elongated and covered by a myelin sheath, a fatty substance that insulates and speeds up the transmission of electrical signals along the axon. The myelin sheath is produced by specialized glial cells called oligodendrocytes in the central nervous system (CNS) and Schwann cells in the peripheral nervous system (PNS).

2. Function: Axons transmit nerve signals, also known as action potentials or nerve impulses, from the cell body to other neurons, muscles, or glands. These signals allow for communication between different parts of the nervous system and facilitate various physiological processes.

3. Synaptic Connections: Axons form synapses, which are specialized junctions with other neurons, muscle cells, or gland cells. At the synapse, the electrical signal is transmitted to the target cell either chemically (by releasing neurotransmitters) or electrically (through gap junctions).

4. Neural Networks: Neurons in the brain often have extensive branching of their axons, allowing them to form complex networks and circuits. These networks underlie various cognitive functions, behaviors, and bodily processes.

5. Propagation of Signals: The transmission of signals along axons occurs through the movement of ions (charged particles) across the cell membrane. This creates an electrical potential difference known as the action potential, which travels down the axon as a wave of depolarization.

6. Speed of Transmission: The speed at which signals travel along axons can vary depending on factors such as the diameter of the axon and the presence of myelin. Myelinated axons conduct signals more rapidly than unmyelinated axons.

7. Axon Regeneration: In the event of damage to the axon, some neurons have the capacity to regenerate to a limited extent, especially in the peripheral nervous system. However, axon regeneration in the central nervous system is generally more challenging due to factors that inhibit regrowth.

Axons are essential components of the nervous system, and their proper function is critical for normal physiological and cognitive processes. Disruptions in axonal communication can lead to a wide range of neurological disorders and conditions.

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"Empowering stroke survivors with cutting-edge neurotherapies."

 

It seems like you're interested in learning about empowering stroke survivors or perhaps advancements in stroke rehabilitation. Stroke is a medical condition that occurs when there is a disruption in blood flow to the brain, leading to damage and potentially causing a range of physical and cognitive impairments. Empowering stroke survivors involves providing them with the tools, resources, and support they need to regain independence, improve their quality of life, and manage the challenges they face after a stroke. Here are some ways in which stroke survivors can be empowered:

1. Comprehensive Rehabilitation: Stroke survivors often require rehabilitation to regain lost functions. Physical therapy, occupational therapy, and speech therapy can help them regain mobility, improve fine motor skills, and overcome communication difficulties.

2. Education and Information: Providing stroke survivors and their families with accurate and understandable information about the condition, recovery process, and available resources can empower them to make informed decisions about their care and lifestyle adjustments.

3. Support Groups: Connecting stroke survivors with support groups or online communities can help them share experiences, exchange advice, and offer emotional support. Interacting with others who have gone through similar experiences can reduce feelings of isolation.

4. Assistive Devices and Technology: Utilizing assistive devices and technology can enhance independence and quality of life. These may include mobility aids, communication devices, and apps designed to aid memory and cognitive function.

5. Lifestyle Modifications: Empowering stroke survivors involves helping them make necessary lifestyle changes, such as adopting a healthy diet, engaging in regular physical activity, managing stress, and avoiding risk factors that could lead to further strokes.

6. Setting Realistic Goals: Encouraging stroke survivors to set achievable goals, both short-term and long-term, can provide a sense of purpose and motivation. Celebrating small victories along the way can boost confidence and self-esteem.

7. Family and Caregiver Support: Involving family members and caregivers in the rehabilitation process is essential. They can provide emotional support, assist with daily activities, and ensure a safe and supportive environment.

8. Psychological Support: Stroke survivors may experience emotional challenges, such as depression, anxiety, or frustration. Access to mental health professionals or counselors can help them address these issues and develop coping strategies.

9. Advancements in Stroke Rehabilitation: Medical advancements, such as neuroplasticity-based therapies, virtual reality rehabilitation, and brain-computer interfaces, are continuously being researched to improve stroke rehabilitation outcomes.

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"Neurogenetics: Linking genes to neurological destinies."

Neurogenetics is a branch of genetics that focuses on understanding the genetic basis of the development, function, and disorders of the nervous system. It explores the relationship between genes, the brain, and behavior, aiming to uncover how genetic variations contribute to various neurological conditions and traits.

Key aspects of neurogenetics include:

Genetic Variation: Neurogeneticists study the variations in genes that are associated with neurological traits and disorders. These variations can involve single nucleotide changes (SNPs), copy number variations (CNVs), or larger structural alterations in the genome.


Neurological Disorders: Neurogenetics plays a crucial role in uncovering the genetic basis of various neurological disorders, such as Alzheimer's disease, Parkinson's disease, autism spectrum disorders, epilepsy, and schizophrenia. Researchers aim to identify specific genes or genetic mutations that increase the risk of developing these conditions.


Heritability of Traits: Many behavioral and cognitive traits have a genetic component. Neurogenetics investigates the heritability of traits such as intelligence, personality, and memory, seeking to understand how genes influence these complex characteristics.


Molecular Mechanisms: Neurogenetic research delves into the molecular mechanisms underlying brain development, function, and plasticity. It explores how genes and proteins regulate neural circuits, synaptic connections, and neurotransmitter systems.


Animal Models: Scientists often use animal models, such as mice and fruit flies, to study neurogenetics. By manipulating genes in these models, researchers can gain insights into the roles of specific genes in neural development and function.


Genetic Testing and Counseling: Advances in neurogenetics have led to the development of genetic tests that can identify individuals at risk for certain neurological disorders. Genetic counseling helps individuals and families understand their genetic predispositions and make informed decisions about their health.


Precision Medicine: Neurogenetics contributes to the emerging field of precision medicine, where treatments are tailored to an individual's genetic makeup. By understanding the genetic factors contributing to neurological disorders, researchers can develop targeted therapies.


Ethical Considerations: Neurogenetics raises important ethical questions, such as those related to privacy, consent, and potential misuse of genetic information. These considerations are especially relevant as genetic testing becomes more accessible

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"Bringing hope to those with neurological disorders."

 

 

Neurological disorders are a broad category of medical conditions that affect the nervous system, which includes the brain, spinal cord, and peripheral nerves. These disorders can have a wide range of symptoms and can impact various aspects of a person's physical and mental health. Here are some examples of neurological disorders:

• Alzheimer's Disease: A progressive neurodegenerative disorder that primarily affects memory, thinking, and behavior. It is the most common cause of dementia.

• Parkinson's Disease: A chronic disorder that affects movement, causing tremors, stiffness, and difficulty with balance and coordination.

• Multiple Sclerosis (MS): An autoimmune disorder where the immune system attacks the protective covering of nerve fibers, leading to communication problems between the brain and the rest of the body.

• Epilepsy: A neurological disorder characterized by recurring seizures, which are abnormal bursts of electrical activity in the brain.

• Migraine: A severe headache disorder often accompanied by other symptoms such as visual disturbances, nausea, and sensitivity to light and sound.

• Amyotrophic Lateral Sclerosis (ALS): Also known as Lou Gehrig's disease, ALS is a progressive neurodegenerative disorder that affects nerve cells in the brain and spinal cord, leading to muscle weakness and loss of motor control.

• Huntington's Disease: An inherited disorder that causes the progressive breakdown of nerve cells in the brain, leading to motor dysfunction, cognitive decline, and psychiatric symptoms.

• Cerebral Palsy: A group of disorders that affect movement, muscle tone, and posture, often caused by brain damage during early development.

• Tourette Syndrome: A neurological disorder characterized by repetitive, involuntary movements and vocalizations called tics.

• Stroke: A sudden interruption of blood supply to the brain, leading to brain damage and often resulting in various neurological deficits.

• Neuropathy: A general term for conditions that affect the peripheral nerves, leading to symptoms like numbness, tingling, pain, and weakness.

• Autism Spectrum Disorder: A developmental disorder that affects communication, behavior, and social interactions.

• Schizophrenia: A complex mental disorder that affects thinking, emotions, and behavior, often involving distorted perceptions of reality.

• Traumatic Brain Injury (TBI): Damage to the brain caused by an external force, often resulting from accidents or falls.

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International Conference on Neurology and Neuro Disorders

 

5th Edition of Neurology | 21-23 August 2023 | Berlin, Germany



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Top US Neurology, Neurosurgery Hospitals Ranked

NYU Langone Hospitals in New York City is once again the best US hospital for neurology care, according to the 2023-2024 US News & World Report's annual ranking of best hospitals for neurology and neurosurgery.

As previously reported by Medscape Medical News, NYU Langone also claimed the top spot in last year’s ranking.

In the latest rankings, UCSF Health-UCSF Medical Center, San Francisco, California, holds the number two spot and New York-Presbyterian Hospital–Columbia and Cornell in New York City holds the number three spot for neurology care, with no change from last year.


This year, Mayo Clinic, Rochester, Minnesota, is ranked number four in neurology and neurosurgery care, up from number six last year, while Cedars-Sinai Medical Center, Los Angeles, California, ranks fifth this year, rising two spots from number seven last year.
Honor Roll

This year, as in prior years, US News also recognized "honor roll" hospitals that have excelled across multiple areas of care. However, this year, for the first time, there is no ordinal ranking of hospitals making the honor roll. Instead, they are listed in alphabetical order.

In a letter to hospital leaders, US News explains that the major change in format came after months of deliberation, feedback from healthcare organizations and professionals, and an analysis of how consumers navigate their website.

Ordinal ranking of hospitals that make the honor roll "obscures the fact that all of the Honor Roll hospitals have attained the highest standard of care in the nation," the letter reads.

This year there are 22 honor roll hospitals.

2023-2024 Honor Roll Hospitals

• Barnes-Jewish Hospital, St. Louis, Missouri

• Brigham and Women’s Hospital, Boston, Massachusetts

• Cedars-Sinai Medical Center, Los Angeles, California

• Cleveland Clinic, Cleveland, Ohio

• Hospitals of the University of Pennsylvania-Penn Medicine, Philadelphia

• Houston Methodist Hospital, Houston, Texas

• Johns Hopkins Hospital, Baltimore, Maryland

• Massachusetts General Hospital, Boston

• Mayo Clinic, Rochester, Minnesota

• Mount Sinai Hospital, New York City

• New York-Presbyterian Hospital-Columbia and Cornell, New York City

• North Shore University Hospital at Northwell Health, Manhasset, New York

• Northwestern Memorial Hospital, Chicago, Illinois

• NYU Langone Hospitals, New York City

• Rush University Medical Center, Chicago, Illinois

• Stanford Health Care-Stanford Hospital, Stanford, California

• UC San Diego Health-La Jolla and Hillcrest Hospitals, California

• UCLA Medical Center, Los Angeles, California

• UCSF Health-UCSF Medical Center, San Francisco, California

• University of Michigan Health-Ann Arbor

• UT Southwestern Medical Center, Dallas, Texas

• Vanderbilt University Medical Center, Nashville, Tennessee

US News notes that to keep pace with consumers’ needs and the ever-evolving landscape of healthcare, "several refinements" are reflected in the latest best hospitals rankings.


These include the introduction of outpatient outcomes in key specialty rankings and surgical ratings, the expanded inclusion of other outpatient data, an increased weight on objective quality measures, and a reduced weight on expert opinion.


In addition, hospital profiles on US News & World Report: News, Rankings and Analysis on Politics, Education, Healthcare and More feature refined health equity measures, including a new measure of racial disparities in outcomes.


Rounding out the top 10 hospitals for neurology and neurosurgery (in order) are UCLA Medical Center, Los Angeles, Johns Hopkins Hospital, Baltimore, Maryland, Massachusetts General Hospital, Boston, Mount Sinai Hospital, New York, and Northwestern Medicine-Northwestern Memorial Hospital, Chicago, Illinois.


US News evaluated 1245 hospitals and ranked the top 50 that treat patients with challenging neurological issues including stroke, conditions affecting the central nervous system, spinal disorders and injuries, seizures, and degenerative nervous system diagnoses such as multiple sclerosis.


"Consumers want useful resources to help them assess which hospital can best meet their specific care needs," Ben Harder, chief of health analysis and managing editor at US News, said in a statement.

"The 2023-2024 Best Hospitals rankings offer patients and the physicians with whom they consult a data-driven source for comparing performance in outcomes, patient satisfaction, and other metrics that matter to them," Harder said.

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Different Types of Myopathies

Did you know that the word “myopathy” is made up of the Greek word “myo” meaning muscle and “pathos” meaning disease? Together, the word myopathy translates to muscle disease and this term is used to describe neuromuscular disorders that primarily cause muscle weakness due to dysfunctional muscle fibers responsible for voluntary motions. Along with muscle weakness, myopathies can also cause muscle cramps, stiffness, spasms, and pain or soreness. There are a variety of myopathies, however they can be broken down into two groups: hereditary and acquired myopathies.
Hereditary Myopathies



Like their name suggests, hereditary myopathies are inherited from an immediate family member. Hereditary myopathies that occur on the X chromosome tend to affect more men than women, while hereditary myopathies that occur on non-sex chromosomes affect men and women equally.

MUSCULAR DYSTROPHIES


Muscular dystrophies are characterized by a lack of protein called dystrophin. Since this protein is essential for normal muscle function, its absence causes muscle damage and weakness that causes problems with walking, swallowing, and muscle coordination.

CONGENITAL MYOPATHY

Congenital myopathies are present at birth, however they may not be diagnosed until later in infancy or early childhood. They are caused by genetic abnormalities in the genes responsible for proper muscle development.

METABOLIC MYOPATHY

Metabolic myopathies are characterized by an inability to properly convert food into energy. Specifically, individuals with metabolic myopathy lack a particular enzyme entirely or are deficient in an enzyme that is required for metabolism. Therefore, the end result is that the muscles are unable to function properly because they are not able to metabolize the required amount of energy.

MITOCHONDRIAL MYOPATHY

Mitochondrial myopathies are characterized by a variety of symptoms all over the body due to the fact that mitochondria exists in cells all over the body. These myopathies are caused by a genetic mutation that affects the cell’s blueprint for making the proteins associated with chemical energy for biochemical reactions. Since muscles require a large amount of energy to function properly, reduced energy will reduce their functionality.

CHANNELOPATHIES

Channelopathies are caused by genetic mutations that impair the function of ion channel units, as well as the proteins responsible for regulating these channels.

MYOTONIA CONGENITA

Myotonia congenita is a type of channelopathy characterized by delayed muscle relaxation and stiffness. In some cases, the disease can even cause muscle enlargement and increased muscle strength. Myotonias are caused by a genetic defect in the genes associated with chloride channels. Chloride channels are used by the body to shut down the electrical activity responsible for muscle contraction. However in people with myotonias, the gene responsible for stopping the electrical activity is damaged, allowing muscle contraction to continue.

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Study highlights the potential of cell replacement therapy for Huntington's disease

New research appearing in the journal Nature Biotechnology answers important questions about the viability of treatments that seek to replace diseased and aged cells in the central nervous system with healthy ones. Its findings have implications for a number of neurological and psychiatric disorders-;including Huntington's disease, amyotrophic lateral sclerosis (ALS), and schizophrenia-;that have been linked to glia, a population of cells that support brain health and function.

The new study from the URMC Center for Translational Neuromedicine, which Goldman co-rects, describes the ability of human glial progenitor cells–precursor cells that can give rise to both astrocytes and oligodendrocytes, the two major types of glia-;to compete with one another in the adult brain, and the competitive advantage of young and healthy cells over aged and diseased cells.

The culmination of a decade of scientific progress

A number of recent important advances are behind the new findings. In 2013, Goldman and colleagues first reported strategies for producing the brain's glial support cells from embryonic stem cells. In later research, the lab transplanted these cells into the brains of baby mice, resulting in the creation of human glial-chimeric mice, a technical achievement that enables the researchers to study human glial cells in the living brain. The team showed that after transplantation, the human glial progenitor cells quickly outcompeted native cells, resulting in brains with mouse neurons and human glia

In later experiments, the lab transplanted human glial cells with the Huntington's disease (HTT) mutation. They observed that this mutation impaired the function of glial progenitor cells, resulting in poor astrocytes and oligodendrocytes production. The lab also showed that transplanting healthy human glial progenitor cells into mouse models of Huntington's delayed disease progression, reinforcing the importance role that glial dysfunction plays in this still untreatable neurodegenerative disease.

Young and healthy cells outcompete older and sick ones

As these prior studies were limited to the transplant of human cells into the mouse brain, the question remained whether human cells transplanted into another human brain would yield the same type of benefit. The new Nature Biotechnology study strongly suggests that the answer to this question is yes, and highlights the potential value of cell replacement therapies by showing that healthy human glia will outcompete and replace sick human cells.

visit: neurology.pencis.com

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