Posts tagged neurological disorders
Articles and news from the latest research reports.
![Hallucinations with Oliver Sacks, November 9, 8 P.M. EST [Live]
The renown neurologist talks about how the brain creates hallucinations — watch this hour-long discussion live and send questions to him via Twitter (using the hashtag #AskOliver to @WorldSciFest).
The conversation, at Cooper Union in New York City, will canvass the rich cultural history and contemporary science of the hallucinatory experience and will also touch on Sacks’ own early psychedelic forays that helped convince him to dedicate his life to neurology and to write about the myriad riddles of the human mind.
Can’t wait? Listen to the Nature podcast interview with Sacks by Kerri Smith, Nature’s podcast editor. Sacks recounts some interesting drug-induced trips, including one in which he has a philosophical discussion with a spider.](http://40.media.tumblr.com/tumblr_md8lgm6Gsm1rog5d1o1_500.jpg)
Hallucinations with Oliver Sacks, November 9, 8 P.M. EST [Live]
The renown neurologist talks about how the brain creates hallucinations — watch this hour-long discussion live and send questions to him via Twitter (using the hashtag #AskOliver to @WorldSciFest).
The conversation, at Cooper Union in New York City, will canvass the rich cultural history and contemporary science of the hallucinatory experience and will also touch on Sacks’ own early psychedelic forays that helped convince him to dedicate his life to neurology and to write about the myriad riddles of the human mind.
Can’t wait? Listen to the Nature podcast interview with Sacks by Kerri Smith, Nature’s podcast editor. Sacks recounts some interesting drug-induced trips, including one in which he has a philosophical discussion with a spider.
(Source: scientificamerican.com)
Oliver Sacks has made a literary art of staring into the minds of others. So what does he make of his own?
Seeing Things? Hearing Things? Many of Us Do
are very startling and frightening: you suddenly see, or hear or smell something — something that is not there. Your immediate, bewildered feeling is, what is going on? Where is this coming from? The hallucination is convincingly real, produced by the same neural pathways as actual perception, and yet no one else seems to see it. And then you are forced to the conclusion that something — something unprecedented — is happening in your own brain or mind. Are you going insane, getting , having a ?
In other cultures, hallucinations have been regarded as gifts from the gods or the Muses, but in modern times they seem to carry an ominous significance in the public (and also the medical) mind, as portents of severe mental or neurological disorders. Having hallucinations is a fearful secret for many people — millions of people — never to be mentioned, hardly to be acknowledged to oneself, and yet far from uncommon. The vast majority are benign — and, indeed, in many circumstances, perfectly normal. Most of us have experienced them from time to time, during a or with the sensory monotony of a desert or empty road, or sometimes, seemingly, out of the blue.
Many of us, as we lie in bed with closed eyes, awaiting sleep, have so-called hypnagogic hallucinations — geometric patterns, or faces, sometimes landscapes. Such patterns or scenes may be almost too faint to notice, or they may be very elaborate, brilliantly colored and rapidly changing — people used to compare them to slide shows.
Researchers identify gene required for nerve regeneration
A gene that is associated with regeneration of injured nerve cells has been identified by scientists at Penn State and Duke University. The team, led by Melissa Rolls, an assistant professor of biochemistry and molecular biology at Penn State, has found that a mutation in a single gene can entirely shut down the process by which axons — the parts of the nerve cell that are responsible for sending signals to other cells — regrow themselves after being cut or damaged. “We are hopeful that this discovery will open the door to new research related to spinal-cord and other neurological disorders in humans,” Rolls said. The journal Cell Reports published an early online copy of the paper (Nov. 1), and also will include the paper in the monthly issue of the journal, which will be published Nov. 29.
Researchers at the doorstep of stem cell therapies for MS, other myelin disorders
When the era of regenerative medicine dawned more than three decades ago, the potential to replenish populations of cells destroyed by disease was seen by many as the next medical revolution. However, what followed turned out not to be a sprint to the clinic, but rather a long tedious slog carried out in labs across the globe required to master the complexity of stem cells and then pair their capabilities and attributes with specific diseases.
In a review article appearing today in the journal Science, University of Rochester Medical Center scientists Steve Goldman, M.D., Ph.D., Maiken Nedergaard, Ph.D., and Martha Windrem, Ph.D., contend that researchers are now on the threshold of human application of stem cell therapies for a class of neurological diseases known as myelin disorders – a long list of diseases that include conditions such as multiple sclerosis, white matter stroke, cerebral palsy, certain dementias, and rare but fatal childhood disorders called pediatric leukodystrophies.
"Stem cell biology has progressed in many ways over the last decade, and many potential opportunities for clinical translation have arisen," said Goldman. "In particular, for diseases of the central nervous system, which have proven difficult to treat because of the brain’s great cellular complexity, we postulated that the simplest cell types might provide us the best opportunities for cell therapy."
The common factor in myelin disorders is a cell called the oligodendrocyte. These cells arise, or are created, by another cell found in the central nervous system called the glial progenitor cell. Both oligodendrocytes and their “sister cells” – called astrocytes – share this same parent and serve critical support functions in the central nervous systems.
(Source: eurekalert.org)
Scientists deepen genetic understanding of MS
Five scientists, including two from Simon Fraser University, have discovered that 30 per cent of our likelihood of developing Multiple Sclerosis (MS) can be explained by 475,806 genetic variants in our genome. Genome-wide Association Studies (GWAS) commonly screen these variants, looking for genetic links to diseases.
Corey Watson, a recent SFU doctoral graduate in biology, his thesis supervisor SFU biologist Felix Breden and three scientists in the United Kingdom have just had their findings published online in Scientific Reports. It’s a sub-publication of the journal Nature.
An inflammatory disease of the central nervous system, MS is the most common neurological disorder among young adults. Canada has one of the highest MS rates in the world.
Watson and his colleagues recently helped quantify MS genetic susceptibility by taking a closer look at GWAS-identified variants in the major histocompatibility complex (MHC) region in 1,854 MS patients. The region has long been associated with MS susceptibility.
The MS patients’ variants were compared to those of 5,164 controls, people without MS.
They noted that eight percent of our 30-per-cent genetic susceptibility to MS is linked to small DNA variations on chromosome 6, which have also long been associated with MS susceptibility.
The MHC encodes proteins that facilitate communication between certain cells in the immune system. Outside of the MHC, a good majority of genetic susceptibility can’t be nailed down because current studies don’t allow for all variants in our genome to be captured.
“Much of the liability is unaccounted for because current research methods don’t enable us to fully interrogate our genome in the context of risk for MS or other diseases,” says Watson.
The researchers believe that one place to look for additional genetic causes of MS may be in genes that have variants that are rare in the population. “The importance of rare gene variants in MS has been illustrated in two recent studies,” notes Watson, now a postdoctoral researcher at the Mount Sinai School of Medicine in New York.
“But these variants, too, are generally poorly represented by genetic markers captured in GWAS, like the one our study was based on.”
(Source: sfu.ca)
BUSM Study Identifies Pathology of Huntington’s Disease
A study led by researchers at Boston University School of Medicine (BUSM) provides novel insight into the impact that Huntington’s disease has on the brain. The findings, published online in Neurology, pinpoint areas of the brain most affected by the disease and opens the door to examine why some people experience milder forms of the disease than others.
Richard Myers, PhD, professor of neurology at BUSM, is the study’s lead/corresponding author. This study, which is the largest to date of brains specific to Huntington’s disease, is the product of nearly 30 years of collaboration between the lead investigators at BUSM and their colleagues at the McLean Brain Tissue Resource Center, Massachusetts General Hospital and Columbia University.
Huntington’s disease (HD) is an inherited and fatal neurological disorder that typically is diagnosed when a person is approximately 40 years old. The gene responsible for the disease was identified in 1993, but the reason why certain neurons or brain cells die remains unknown.
The investigators examined 664 autopsy brain samples with HD that were donated to the McLean Brain Bank. They evaluated and scored more than 50 areas of the brain for the effects of HD on neurons and other brain cell types. This information was combined with a genetic study to characterize variations in the Huntington gene. They also gathered the clinical neurological information on the patients’ age when HD symptoms presented and how long the patient survived with the disease.
Based on this analysis, the investigators discovered that HD primarily damages the brain in two areas. The striatum, which is located deep within the brain and is involved in motor control and involuntary movement, was the area most severely impacted by HD. The outer cortical regions, which are involved in cognitive function and thought processing, also showed damage from HD, but it was less severe than in the striatum.
The investigators identified extraordinary variation in the extent of cell death in different brain regions. For example, some individuals had extremely severe outer cortical degeneration while others appeared virtually normal. Also, the extent of involvement for these two regions was remarkably unrelated, where some people demonstrated heavy involvement in the striatum but very little involvement in the cortex, and vice versa.
“There are tremendous differences in how people with Huntington’s disease are affected,” Myers said. “Some people with the disease have more difficulty with motor control than with their cognitive function while others suffer more from cognitive disability than motor control issues.”
When studying these differences, the investigators noted that the cell death in the striatum is heavily driven by the effects of variations in the Huntington gene itself, while effects on the cortex were minimally affected by the HD gene and are thus likely to be a consequence of other unidentified causes. Importantly, the study showed that some people with HD experienced remarkably less neuronal cell death than others.
“While there is just one genetic defect that causes Huntington’s disease, the disease affects different parts of the brain in very different ways in different people,” said Myers. “For the first time, we can measure these differences with a very fine level of detail and hopefully identify what is preventing brain cell death in some individuals with HD.”
The investigators have initiated extensive studies into what genes and other factors are associated with the protection of neurons in HD, and they hope these protective factors will point to possible novel treatments.
(Source: bumc.bu.edu)
Attack! Silent watchmen charge to defend the nervous system
In many pathologies of the nervous system, there is a common event - cells called microglia are activated from surveillant watchmen into fighters. Microglia are the immune cells of the nervous system, ingesting and destroying pathogens and damaged nerve cells. Until now little was known about the molecular mechanisms of microglia activation despite this being a critical process in the body. Now new research from the Montreal Neurological Institute and Hospital – The Neuro - at McGill University provides the first evidence that mechanisms regulated by the Runx1 gene control the balance between the surveillant versus activated microglia states. The finding, published in the Journal of Neuroscience, has significant implications for understanding and treating neurological conditions.
How Neuroscience is Changing the Talking Cure
What’s the Latest Development?
A new book which attempts to reconcile psychoanalysis with neuroscience may have practical implications in the treatment of neurological disorders such as Alzheimer’s and PTSD. Catherine Malabou’s What Should We Do With Our Brain? argues that “we have failed to understand ourselves because we have failed to acknowledge recent scientific discoveries, particularly ‘plasticity,’ or the brain’s ability to change.” Through the course of the argument, Malabou updates psychotherapy’s concept of clinical treatment by recognizing that mental wounds do not come from a buried subconscious but from events that befall us in the real world.
What’s the Big Idea?
Malabou references clinical trials with patients who have acquired neurological disorders (rather than being born with them) and finds that patients do not identify with a stable psyche—the sort required by traditional psychological investigation. Rather, patients experience themselves as a different person, one with whom they are unfamiliar. “The old onion of the psyche, with its layers upon layers of meaning, is simply not there to peel apart in analysis; rather, it has been replaced by a new self, which requires a different clinical approach.”
NIH researchers provide detailed view of brain protein structure
Results may help improve drugs for neurological disorders
Researchers have published the first highly detailed description of how neurotensin, a neuropeptide hormone which modulates nerve cell activity in the brain, interacts with its receptor. Their results suggest that neuropeptide hormones use a novel binding mechanism to activate a class of receptors called G-protein coupled receptors (GPCRs).
“The knowledge of how the peptide binds to its receptor should help scientists design better drugs,” said Dr. Reinhard Grisshammer, a scientist at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS) and an author of the study published in Nature.
Binding of neurotensin initiates a series of reactions in nerve cells. Previous studies have shown that neurotensin may be involved in Parkinson’s disease, schizophrenia, temperature regulation, pain, and cancer cell growth.
Dr. Grisshammer and his colleagues used X-ray crystallography to show what the receptor looks like in atomic detail when it is bound to neurotensin. Their results provide the most direct and detailed views describing this interaction which may change the way scientists develop drugs targeting similar neuropeptide receptors.
X-ray crystallography is a technique in which scientists shoot X-rays at crystallized molecules to determine a molecule’s shape and structure. The X-rays change directions, or diffract, as they pass through the crystals before hitting a detector where they form a pattern that is used to calculate the atomic structure of the molecule. These structures guide the way scientists think about how proteins work.
Neurotensin receptors and other GPCRs belong to a large class of membrane proteins which are activated by a variety of molecules, called ligands. Previous X-ray crystallography studies showed that smaller ligands, such as adrenaline and retinal, bind in the middle of their respective GPCRs and well below the receptor’s surface. In contrast, Dr. Grisshammer’s group found that neurotensin binds to the outer part of its receptor, just at the receptor surface. These results suggest that neuropeptides activate GPCRs in a different way compared to the smaller ligands.
Forming well-diffracting neuropeptide-bound GPCR crystals is very difficult. Dr. Grisshammer and his colleagues spent many years obtaining the results on the neurotensin receptor. During that time Dr. Grisshammer started collaborating with a group led by Dr. Christopher Tate, Ph.D. at the MRC Laboratory of Molecular Biology, Cambridge, England. Dr. Tate’s lab used recombinant gene technology to create a stable version of the neurotensin receptor which tightly binds neurotensin. Meanwhile Dr. Grisshammer’s lab employed the latest methods to crystallize the receptor bound to a short version of neurotensin.
The results published today are the first X-ray crystallography studies showing how a neuropeptide agonist binds to neuropeptide GPCRs. Nonetheless, more work is needed to fully understand the detailed signaling mechanism of this GPCR, said Dr. Grisshammer.
(Source: ninds.nih.gov)