Topic Review
Neurodegeneration in Multiple Sclerosis
Neurodegeneration in multiple sclerosis is believed to underlie disease progression and permanent disability. Many mechanisms of neurodegeneration in MS have been proposed, such as mitochondrial dysfunction, oxidative stress, neuroinflammation, and most recently RNA-binding protein dysfunction. Studying RNA-binding protein dysfunction addresses a gap in our understanding of the pathogenesis of MS, which may allow for novel therapies to be generated to attenuate neurodegeneration before irreversible central nervous system damage occurs.
  • 487
  • 29 Jun 2021
Topic Review
Essential Oils and Neurodegenerative Diseases
Despite the improvements in life expectancy, neurodegenerative conditions have arguably become the most dreaded maladies of older people. The neuroprotective and anti-ageing potentials of essential oils (EOs) are widely evaluated around the globe. The entry focuses on analysing the effectiveness of EOs as neuroprotective remedies among the four common age-related neurodegenerative diseases. The literature was extracted from three databases (PubMed, Web of Science and Google Scholar) between the years of 2010 to 2020 using the medical subject heading (MeSH) terms “essential oil”, crossed with “Alzheimer’s disease (AD)”, “Huntington’s disease (HD)”, “Parkinson’s disease (PD)” or “amyotrophic lateral sclerosis (ALS)”. Eighty three percent (83%) of the studies were focused on AD, while another 12% focused on PD. No classifiable study was recorded on HD or ALS. EO from Salvia officinalis has been recorded as one of the most effective acetylcholinesterase and butyrylcholinesterase inhibitors. However, only Cinnamomum sp. has been assessed for its effectiveness in both AD and PD. 
  • 471
  • 31 Mar 2021
Topic Review
FDA-Approved Multiple Sclerosis Drugs
The molecular effects of traditional and more recently FDA-approved Multiple Sclerosis (MS) drugs on four CNS cell types.
  • 443
  • 26 Oct 2020
Topic Review
Neuron Migration
Radial neuron migration in the developing cerebral cortex is a complex journey, starting in the germinal zones and ending in the cortical plate. In mice, migratory distances can reach several hundreds of microns, or millimeters in humans. Along the migratory path, radially migrating neurons slither through cellularly dense and complex territories before they reach their final destination in the cortical plate.
  • 428
  • 06 Jan 2021
Topic Review
Paroxysmal Movement Disorders
Paroxysmal movement disorders (PMDs) are rare neurological diseases typically manifesting with intermittent attacks of abnormal involuntary movements.
  • 406
  • 06 Nov 2020
Topic Review
Huntington’s Disease
Huntington’s disease (HD) is an autosomal dominant neurodegenerative disorder caused by pathogenic expansions of the triplet cytosine-adenosine-guanosine (CAG) within the Huntingtin gene. These expansions lead to a prolongation of the poly-glutamine stretch at the N-terminus of Huntingtin causing protein misfolding and aggregation. Huntingtin and its pathological variants are widely expressed, but the central nervous system is mainly a ected, as proved by the wide spectrum of neurological symptoms, including behavioral anomalies, cognitive decline and motor disorders. Other hallmarks of HD are loss of body weight and muscle atrophy. This review highlights some key elements that likely provide a major contribution to muscle atrophy, namely, alteration of the transcriptional processes, mitochondrial dysfunction, which is strictly correlated to loss of energy homeostasis, inflammation, apoptosis and defects in the processes responsible for the protein quality control. The improvement of muscular symptoms has proven to slow the disease progression and extend the life span of animal models of HD, underlining the importance of a deep comprehension of the molecular mechanisms driving deterioration of muscular tissue.
  • 355
  • 24 Nov 2020
Topic Review
C-reactive protein (CRP) apheresis
Almost every kind of inflammation in the human body is accompanied by rising C-reactive protein (CRP) concentrations. This can include bacterial and viral infection, chronic inflammation and so-called sterile inflammation triggered by (internal) acute tissue injury. CRP is part of the ancient humoral immune response and secreted into the circulation by the liver upon respective stimuli. Its main immunological functions are the opsonization of biological particles (bacteria and dead or dying cells) for their clearance by macrophages and the activation of the classical complement pathway. This not only helps to eliminate pathogens and dead cells, which is very useful in any case, but unfortunately also to remove only slightly damaged or inactive human cells that may potentially regenerate with more CRP-free time. CRP action severely aggravates the extent of tissue damage during the acute phase response after an acute injury and therefore negatively affects clinical outcome. CRP is therefore a promising therapeutic target to rescue energy-deprived tissue either caused by ischemic injury (e.g., myocardial infarction and stroke) or by an overcompensating immune reaction occurring in acute inflammation (e.g., pancreatitis) or systemic inflammatory response syndrome (SIRS; e.g., after transplantation or surgery). Selective CRP apheresis can remove circulating CRP safely and efficiently. We explain the pathophysiological reasoning behind therapeutic CRP apheresis and summarize the broad span of indications in which its application could be beneficial with a focus on ischemic stroke as well as the results of this therapeutic approach after myocardial infarction.
  • 354
  • 17 Sep 2020
Topic Review
Gangliosidoses
Gangliosides are sialic acid containing complex glycolipids, anchored and enriched in the outer leaflet of neuronal plasma membranes, with their glycan chains facing the extracellular space. Undegradeable gangliosides and related glycosphingolipids and oligosaccharides accumulate progressively  in fatal lysosomal storage diseases, originally described as infantile amaurotic idiocy. Their lysosomal storage is caused by specific monogenic defects of catabolic hydrolyses or ancillary lipid-binding and -transfer proteins, essential for specific steps in their lysosomal catabolism.  However, small gangliosides can also accumulate as secondary material in other lysosomal storage diseases without a known defect in their catabolic pathway. Primary storage material of such diseases, sphingomyelin, lysosphingolipids, cholesterol and chondroitin sulfate are efficient inhibitors of specific steps of ganglioside catabolic pathway. They  can attenuate ganglioside turnover, assisted by lipid binding proteins, the GM2 activator protein (GM2AP) and saposin B
  • 341
  • 29 Oct 2020
Topic Review
Stem Cell Therapy
Neurodegenerative diseases resulting from the progressive loss of structure and/or function of neurons contribute to different paralysis degrees and loss of cognition and sensation. The lack of successful curative therapies for neurodegenerative disorders leads to a considerable burden on society and a high economic impact. Over the past 20 years, regenerative cell therapy, also known as stem cell therapy, has provided an excellent opportunity to investigate potentially powerful innovative strategies for treating neurodegenerative diseases.
  • 340
  • 08 Mar 2021
Topic Review
Magnetoencephalography
Magnetoencephalography (MEG) is a functional brain imaging technique that measures magnetic flux on the surface of the head associated with underlying neuronal electrical dipoles.
  • 330
  • 08 Mar 2021
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