102 results match your criteria Future Neurology[Journal]


New directions in therapeutics for Huntington disease.

Future Neurol 2018 May 29;13(2):101-121. Epub 2018 May 29.

Professor Emeritus, Department of Psychiatry & Human Behavior, University of California, Irvine, CA 92697, USA.

Huntington disease (HD) is an autosomal dominantly inherited neurodegenerative disease that affects motor, cognitive and psychiatric functions, and ultimately leads to death. The pathology of the disease is based on an expansion of CAG repeats in exon 1 of the gene on chromosome 4, which produces a mutant huntingtin protein (mHtt). This protein is involved in neurotoxicity and brain atrophy, and can form β-sheets and abnormal mHtt aggregates. Read More

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http://dx.doi.org/10.2217/fnl-2017-0035DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6378950PMC
May 2018
2 Reads

The mTOR pathway in treatment of epilepsy: a clinical update.

Future Neurol 2018 May 29;13(2):49-58. Epub 2018 May 29.

Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, USA.

Nearly a third of patients with epilepsy have seizures refractory to current medical therapies. In the search for novel drug targets, the mTOR pathway has emerged as key in the regulation of neuronal function, growth and survival, and other cellular processes related to epileptogenesis. Hyperactivation of the mTOR pathway has been implicated in tuberous sclerosis complex and other 'mTORopathies', clinical syndromes associated with cortical developmental malformations and drug-resistant epilepsy. Read More

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http://dx.doi.org/10.2217/fnl-2018-0001DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6261508PMC
May 2018
3 Reads

Comorbid autism spectrum disorder and anxiety disorders: a brief review.

Future Neurol 2018 Feb 17;13(1):31-37. Epub 2018 Jan 17.

Menninger Department of Psychiatry & Behavioral Sciences, Baylor College of Medicine, Houston, TX 77030, USA.

Appearing in 40% of the cases of autism spectrum disorder (ASD), comorbid anxiety presents unique challenges for practitioners by amplifying problem behaviors such as social skills deficits, resistance to change and repetitive behaviors. Furthermore, comorbid ASD/anxiety strains familial relationships and increases parental stress. Research indicates that the neurobiological interactions between anxiety and ASD require comprehensive assessment approaches, modified cognitive behavioral therapy and carefully managed pharmacological interventions. Read More

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http://dx.doi.org/10.2217/fnl-2017-0030DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5772195PMC
February 2018
2 Reads

What goes up must come down: homeostatic synaptic plasticity strategies in neurological disease.

Future Neurol 2018 Feb 17;13(1):13-21. Epub 2018 Jan 17.

Department of Pharmacology & Physiology, Georgetown University Medical Center, Washington DC 20057, USA.

Brain activity levels are tightly regulated to minimize imbalances in activity state. Deviations from the normal range of activity are deleterious and often associated with neurological disorders. To maintain optimal levels of activity, regulatory mechanisms termed homeostatic synaptic plasticity establish desired 'set points' for neural activity, monitor the network for deviations from the set point and initiate compensatory responses to return activity to the appropriate level that permits physiological function [1,2]. Read More

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http://dx.doi.org/10.2217/fnl-2017-0028DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5772176PMC
February 2018
4 Reads

A report of nontraumatic cortical subarachnoid hemorrhage and subsequent management.

Future Neurol 2016 Nov 21;11(4):231-235. Epub 2016 Oct 21.

Kings County Hospital Center, Department of Neurology, 451 Clarkson Ave, Brooklyn, NY 11203, USA.

Aim: Report a case of cortical subarachnoid hemorrhage (cSAH) and discuss its management.

Patient & Methods: A 66-year-old woman presents with acute onset left arm numbness and weakness. Initial head CT shows small hyperdensity in sulci typical for cSAH. Read More

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http://dx.doi.org/10.2217/fnl-2016-0016DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5480783PMC
November 2016
6 Reads

Inositol depletion, GSK3 inhibition and bipolar disorder.

Future Neurol 2016 May 26;11(2):135-148. Epub 2016 Apr 26.

Department of Biological Sciences, Wayne State University, Detroit, MI 48202, USA.

Valproic acid and lithium are widely used to treat bipolar disorder, a severe illness characterized by cycles of mania and depression. However, their efficacy is limited, and treatment is often accompanied by serious side effects. The therapeutic mechanisms of these drugs are not understood, hampering the development of more effective treatments. Read More

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http://dx.doi.org/10.2217/fnl-2016-0003DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5751514PMC
May 2016
2 Reads

CNS autoimmune disease after infections: animal models, cellular mechanisms and genetic factors.

Future Neurol 2016 Dec;11(1):63-76

Department of Neurology, Columbia University Medical Center, 650 West 168 Street, Room 310E, New York, NY 10032, USA; Departments of Pathology & Cell Biology & Pharmacology, Columbia University Medical Center, 650 West 168 Street, Room 310E, New York, NY 10032, USA.

infections have been associated with two autoimmune diseases of the CNS: Sydenham's chorea (SC) and Pediatric Autoimmune Neuropsychiatric Disorders Associated with infections (PANDAS). Despite the high frequency of pharyngeal streptococcus infections among children, only a small fraction develops SC or PANDAS. This suggests that several factors in combination are necessary to trigger autoimmune complications: specific strains that induce a strong immune response toward the host nervous system; genetic susceptibility that predispose children toward an autoimmune response involving movement or tic symptoms; and multiple infections of the throat or tonsils that lead to a robust T17 cellular and humoral immune response when untreated. Read More

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http://dx.doi.org/10.2217/fnl.16.4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4839655PMC
December 2016
57 Reads

Novel susceptibility loci for Alzheimer's disease.

Authors:
Christiane Reitz

Future Neurol 2015 Dec;10(6):547-558

Late-onset Alzheimer's disease (AD), a highly prevalent neurodegenerative disorder characterized by progressive deterioration in cognition, function and behavior terminating in incapacity and death, is a clinically and pathologically heterogeneous disease with a substantial heritable component. During the past 5 years, the technological developments in next-generation high-throughput genome technologies have led to the identification of more than 20 novel susceptibility loci for AD, and have implicated specific pathways in the disease, in particular intracellular trafficking/endocytosis, inflammation and immune response and lipid metabolism. These observations have significantly advanced our understanding of underlying pathogenic mechanisms and potential therapeutic targets. Read More

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http://dx.doi.org/10.2217/fnl.15.42DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4820289PMC
December 2015
8 Reads

The future of stem cell therapy for stroke rehabilitation.

Future Neurol 2015 Aug;10(4):313-319

University Hospital of Grenoble, Stroke Unit, Department of Neurology, CS 10217, 38043 Grenoble, France; Inserm, U 836, BP 170, 38042 Grenoble, France; University Grenoble Alpes, Grenoble Institute of Neurosciences, BP 170, 38042 Grenoble, France.

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http://dx.doi.org/10.2217/FNL.15.27DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4795912PMC
August 2015
7 Reads

Stroke therapy: the potential of amniotic fluid-derived stem cells.

Future Neurol 2015;10(4):321-326

Department of Neurosurgery & Brain Repair, University of South Florida College of Medicine, 12901 Bruce B Downs Blvd, FL 33612, USA ; Center of Excellence for Aging & Brain Repair, Department of Neurosurgery & Brain Repair, University of South Florida Morsani College of Medicine, 12901 Bruce B Downs Blvd, Tampa, FL 33612, USA.

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http://dx.doi.org/10.2217/FNL.15.19DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4577242PMC
January 2015
23 Reads

The hippocampo-prefrontal pathway: a possible therapeutic target for negative and cognitive symptoms of schizophrenia.

Future Neurol 2015;10(2):115-128

Vanderbilt Center for Neuroscience Drug Discovery, Department of Pharmacology, Vanderbilt University Medical Center, Nashville, TN 37232 0697, USA.

The hippocampo-prefrontal (H-PFC) pathway has been linked to cognitive and emotional disturbances in several psychiatric disorders including schizophrenia. Preclinical evidence from the NMDA receptor antagonism rodent model of schizophrenia shows severe pathology selective to the H-PFC pathway. It is speculated that there is an increased excitatory drive from the hippocampus to the prefrontal cortex due to dysfunctions in the H-PFC plasticity, which may serve as the basis for the behavioral consequences observed in this rodent model. Read More

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http://dx.doi.org/10.2217/FNL.14.63DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4376007PMC
January 2015
5 Reads

Anatomical, functional and molecular biomarker applications of magnetic resonance neuroimaging.

Authors:
Christina H Liu

Future Neurol 2015 Jan;10(1):49-65

National Institute of Biomedical Imaging & Bioengineering, 6707 Democracy Blvd, Suite 200, Bethesda, MD 20892, USA; Tel.: +1 301 451 7638;

MRI and magnetic resonance spectroscopy (MRS) along with computed tomography and PET are the most common imaging modalities used in the clinics to detect structural abnormalities and pathological conditions in the brain. MRI generates superb image resolution/contrast without radiation exposure that is associated with computed tomography and PET; MRS and spectroscopic imaging technologies allow us to measure changes in brain biochemistry. Increasingly, neurobiologists and MRI scientists are collaborating to solve neuroscience problems across sub-cellular through anatomical levels. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4354814PMC
January 2015
5 Reads

Management of epilepsy during pregnancy: evidence-based strategies.

Future Neurol 2015 Mar 4;10(2):161-176. Epub 2015 Mar 4.

Department of Neurology, Brigham & Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.

Child-bearing years are often the most precarious management period in the life of a woman with epilepsy. This article reviews the results of many different studies with findings that enable the healthcare team to make confident decisions and recommendations during these critical periods. Preconceptional planning, effective contraception and folic acid supplementation are important fundamentals in preparation for pregnancy. Read More

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http://dx.doi.org/10.2217/FNL.15.4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6376992PMC

Human-derived natural antibodies: biomarkers and potential therapeutics.

Future Neurol 2015;10(1):25-39

Department of Neurology, Mayo Clinic College of Medicine, Rochester, MN 55905, USA ; Department of Immunology, Mayo Clinic College of Medicine, Rochester, MN 55905, USA.

The immune system generates antibodies and antigen-specific T-cells as basic elements of the immune networks that differentiate self from non-self in a finely tuned manner. The antigen-specific nature of immune responses ensures that normal immune activation contains non-self when tolerating self. Here we review the B-1 subset of lymphocytes which produce self-reactive antibodies. Read More

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http://dx.doi.org/10.2217/fnl.14.62DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4321763PMC
January 2015
5 Reads

Facial neuropathy with imaging enhancement of the facial nerve: a case report.

Future Neurol 2014 Nov;9(6):571-576

Comprehensive Stroke Program, Department of Neurology, School of Medicine & Public Health, University of Wisconsin, Medical Foundation Centennial Building,1685 Highland Ave # 7273, Madison, WI 53705-2281, USA.

A young women developed unilateral facial neuropathy 2 weeks after a motor vehicle collision involving fractures of the skull and mandible. MRI showed contrast enhancement of the facial nerve. We review the literature describing facial neuropathy after trauma and facial nerve enhancement patterns with different causes of facial neuropathy. Read More

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http://dx.doi.org/10.2217/fnl.14.55DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4283939PMC
November 2014
6 Reads

Animal models of stroke: translational potential at present and in 2050.

Future Neurol 2014 Sep;9(5):541-551

Department of Pharmacology, University of Colorado Denver, Anschutz Medical Campus, 12800 E 19th Avenue, Aurora, CO 80045, USA ; Department of Anesthesiology, University of Colorado Denver, Anschutz Medical Campus, 12800 E 19th Avenue, Aurora, CO 80045, USA.

Translation from basic science bench research in ischemic stroke to bedside treatment of patients suffering ischemic stroke remains a difficult challenge. Despite literally hundreds of compounds and interventions that provide benefit in experimental models of cerebral ischemia, efficacy in humans remains to be demonstrated. The reasons for failure to translate the extensive positive basic science findings to successful clinical trials have been the focus of discussion for years. Read More

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https://www.futuremedicine.com/doi/10.2217/fnl.14.44
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http://dx.doi.org/10.2217/fnl.14.44DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4266275PMC
September 2014
6 Reads

Genetic loci associated with Alzheimer's disease.

Authors:
Christiane Reitz

Future Neurol 2014 Mar;9(2):119-122

The Taub Institute for Research on Alzheimer's Disease & the Aging Brain, Columbia University, New York, NY, USA and Gertrude H Sergievsky Center, 630 West 168th Street, Columbia University, New York, NY 10032, USA and The Department of Neurology, Columbia University, New York, NY, USA Tel.: +1 212 305 0865; ;

The article by Lambert reports the identification of 11 novel susceptibility loci for late-onset Alzheimer's disease. The observations of this study significantly enhance the field since they further disentangle the genetic causes and pathways underlying Alzheimer's disease by identifying novel disease-associated variants clustering in specific pathways. These pathways include APP processing, lipid metabolism, inflammation/immune response, intracellular trafficking/endocytosis, tau metabolism, synaptic function. Read More

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http://dx.doi.org/10.2217/fnl.14.1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4266532PMC
March 2014
5 Reads

characterization of brain iron with magnetic field correlation imaging.

Future Neurol 2014 May;9(3):247-250

Center for Biomedical Imaging, Department of Radiology & Radiological Science, Medical University of South Carolina, 96 Jonathan Lucas St, MSC 323 Charleston, SC 29425, USA.

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http://dx.doi.org/10.2217/fnl.14.21DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4217209PMC
May 2014
7 Reads

Neuroimaging chronic pain: what have we learned and where are we going?

Future Neurol 2014 Nov;9(6):615-626

Department of Anesthesiology, Perioperative & Pain Medicine, Division of Pain Medicine, Stanford University School of Medicine, 1070 Arastradero Road, Suite 200, Palo Alto, CA 94304, USA.

Advances in neuroimaging have helped illuminate our understanding of how the brain works in the presence of chronic pain, which often persists with unknown etiology or after the painful stimulus has been removed and any wounds have healed. Neuroimaging has enabled us to make great progress in identifying many of the neural mechanisms that contribute to chronic pain, and to pinpoint the specific regions of the brain that are activated in the presence of chronic pain. It has provided us with a new perception of the nature of chronic pain in general, leading researchers to move toward a whole-brain approach to the study and treatment of chronic pain, and to develop novel technologies and analysis techniques, with real potential for developing new diagnostics and more effective therapies. Read More

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http://dx.doi.org/10.2217/FNL.14.57DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5289824PMC
November 2014
9 Reads

Regional variability in Alzheimer's disease biomarkers.

Future Neurol 2014 ;9(2):131-134

Department of Radiology, Washington University in St. Louis.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4192718PMC
January 2014
3 Reads

Translating cerebellar Purkinje neuron physiology to progress in dominantly inherited ataxia.

Future Neurol 2014 Mar;9(2):187-196

Department of Neurology, University of Michigan, Alfred A Taubman Biomedical Science Research Building, Room 4009, 109 Zina Pitcher Place, Ann Arbor, MI 48109-2200, USA.

The cerebellum is an important structure for accurate control and timing of movement, and Purkinje neurons in the cerebellar cortex are key players in cerebellar motor control. Cerebellar dysfunction can result in ataxia, a disorder characterized by postural instability, gait disturbances and motor incoordination. Cerebellar ataxia is a symptom of a number of conditions, and the emerging evidence that Purkinje neuron dysfunction, in particular, abnormal Purkinje neuron repetitive firing, is a major driver of motor dysfunction in a subset of dominantly inherited ataxias is dicussed. Read More

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http://dx.doi.org/10.2217/fnl.14.6DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4159172PMC
March 2014
4 Reads

What have novel imaging techniques revealed about metabolism in the aging brain?

Future Neurol 2014 May;9(3):341-354

Magnetic Resonance Research Center, Diagnostic Radiology & Biomedical Engineering, Yale University, New Haven, CT, USA.

Brain metabolism declines with age and do so in an accelerated manner in neurodegenerative disorders. Noninvasive neuroimaging techniques have played an important role to identify the metabolic biomarkers in aging brain. Particularly, PET with fluorine-18 (F)-labeled 2-fluoro-2-deoxy-d-glucose tracer and proton magnetic resonance spectroscopy (MRS) have been widely used to monitor changes in brain metabolism over time, identify the risk for Alzheimer's disease (AD) and predict the conversion from mild cognitive impairment to AD. Read More

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http://dx.doi.org/10.2217/fnl.14.13DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4159180PMC
May 2014
4 Reads

Towards an Understanding of Neuropsychiatric Manifestations in Fragile X Premutation Carriers.

Future Neurol 2014 Mar;9(2):227-239

Department of Psychiatry, University of California San Francisco School of Medicine, San Francisco, California 94143 USA.

Fragile X-associated disorders (FXD) are a group of disorders caused by expansion of non-coding CGG repeat elements in the fragile X () gene. One of these disorders, fragile X syndrome (FXS), is the most common heritable cause of intellectual disability, and is caused by large CGG repeat expansions (>200) resulting in silencing of the gene. An increasingly recognized number of neuropsychiatric FXD have recently been identified that are caused by 'premutation' range expansions (55-200). Read More

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http://dx.doi.org/10.2217/fnl.14.11DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4086747PMC
March 2014
21 Reads

Migraine and obesity: moving beyond BMI.

Future Neurol 2014 Jan;9(1):37-40

Department of Neurology, Johns Hopkins University School of Medicine, 4940 Eastern Avenue, Baltimore, MD 21224, USA.

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http://dx.doi.org/10.2217/fnl.13.65DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4000031PMC
January 2014
5 Reads

Axonal tract tracing for delineating interacting brain regions: implications for Alzheimer's disease-associated memory.

Future Neurol 2014 Jan;9(1):89-98

Department of Cell, Developmental & Integrative Biology, University of Alabama at Birmingham, 1900 University Boulevard, THT 912, Birmingam, AL 35294-0006, USA.

We are studying the projections from the entorhinal cortex to the hippocampal formation in the mouse. The dentate gyrus is innervated by the lateral entorhinal cortex (lateral perforant path) and medial entorhinal cortex (medial perforant path). The entorhinal cortex also projects to hippocampal areas CA3 and CA1, and to the subiculum. Read More

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http://dx.doi.org/10.2217/fnl.13.67DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3963157PMC
January 2014
3 Reads

Neurodegeneration in spinal muscular atrophy: from disease phenotype and animal models to therapeutic strategies and beyond.

Future Neurol 2014 Jan;9(1):49-65

Department of Neurology, 630 West 168th Street, Columbia University Medical Center, New York, NY 10032, USA ; Center for Motor Neuron Biology & Disease, 630 West 168th Street, Columbia University Medical Center, New York, NY 10032, USA ; Department of Pediatrics, 630 West 168th Street, Columbia University Medical Center, New York, NY 10032, USA.

Of the numerous inherited diseases known to afflict the pediatric population, spinal muscular atrophy (SMA) is among the most common. It has an incidence of approximately one in 10,000 newborns and a carrier frequency of one in 50. Despite its relatively high incidence, SMA remains somewhat obscure among the many neurodegenerative diseases that affect humans. Read More

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http://dx.doi.org/10.2217/fnl.13.58DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3955729PMC
January 2014
6 Reads

Molecular contributions to neurovascular unit dysfunctions after brain injuries: lessons for target-specific drug development.

Future Neurol 2013 Nov;8(6):677-689

Department of Pediatrics, Loma Linda University School of Medicine, Loma Linda, CA 92354, USA ; Department of Physiology, Loma Linda University School of Medicine, Loma Linda, CA 92354, USA.

The revised 'expanded' neurovascular unit (eNVU) is a physiological and functional unit encompassing endothelial cells, pericytes, smooth muscle cells, astrocytes and neurons. Ischemic stroke and traumatic brain injury are acute brain injuries directly affecting the eNVU with secondary damage, such as blood-brain barrier (BBB) disruption, edema formation and hypoperfusion. BBB dysfunctions are observed at an early postinjury time point, and are associated with eNVU activation of proteases, such as tissue plasminogen activator and matrix metalloproteinases. Read More

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http://dx.doi.org/10.2217/fnl.13.55DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3904383PMC
November 2013
10 Reads

Diffusion tensor imaging and related techniques in tuberous sclerosis complex: review and future directions.

Future Neurol 2013 Sep;8(5):583-597

Department of Radiology & the Computational Radiology Laboratory, Boston Children's Hospital, Boston, MA 02115, USA.

In this article, the authors aim to introduce the nonradiologist to diffusion tensor imaging (DTI) and its applications to both clinical and research aspects of tuberous sclerosis complex. Tuberous sclerosis complex is a genetic neurocutaneous syndrome with variable and unpredictable neurological comorbidity that includes refractory epilepsy, intellectual disability, behavioral abnormalities and autism spectrum disorder. DTI is a method for modeling water diffusion in tissue and can noninvasively characterize microstructural properties of the brain. Read More

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http://dx.doi.org/10.2217/fnl.13.37DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3904372PMC
September 2013
5 Reads

Neuronal adhesion and synapse organization in recovery after brain injury.

Future Neurol 2013 Sep;8(5):555-567

Department of Molecular Biophysics & Biochemistry, Yale University School of Medicine, New Haven, CT, USA ; Program in Cellular Neuroscience, Neurodegeneration & Repair, Yale University School of Medicine, New Haven, CT, USA.

Few specific therapeutic targets exist to manage brain injury, despite the prevalence of stroke or traumatic brain injury. With traumatic brain injury, characteristic neuronal changes include axonal swelling and degeneration, and the loss of synapses, the sites of communication between neurons. This is followed by axonal sprouting and alterations in synaptic markers in recovery. Read More

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http://dx.doi.org/10.2217/fnl.13.35DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3905318PMC
September 2013
4 Reads

Inflammation and human cerebral aneurysms: current and future treatment prospects.

Future Neurol 2013 Nov;8(6)

Department of Neurosurgery, University of Iowa Hospitals & Clinics, 200 Hawkins Drive, Iowa City, IA 52240, USA.

The formation of cerebral aneurysms and their rupture propensity is of immediate clinical importance. Current management includes observation with expectant management, microsurgical clipping and/or endovascular coiling. The surgical options are invasive and are not without increased risk despite the technological advances. Read More

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http://dx.doi.org/10.2217/fnl.13.40DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3873146PMC
November 2013
3 Reads

astrocytic Ca signaling in health and brain disorders.

Authors:
Shinghua Ding

Future Neurol 2013 Sep;8(5):529-554

Dalton Cardiovascular Research Center, Department of Biological Engineering, University of Missouri, Columbia, MO 65211, USA

Astrocytes are the predominant glial cell type in the CNS. Although astrocytes are electrically nonexcitable, their excitability is manifested by their Ca signaling, which serves as a mediator of neuron-glia bidirectional interactions via tripartite synapses. Studies from two-photon imaging indicate that in healthy animals, the properties of spontaneous astrocytic Ca signaling are affected by animal species, age, wakefulness and the location of astrocytes in the brain. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3873150PMC
September 2013
4 Reads

Parkinson's Disease: What role do pedunculopontine nucleus cholinergic neurons play?

Future Neurol 2014 Jan 16;9(1):5-8. Epub 2013 Dec 16.

Department of Neurology, University of Michigan, Ann Arbor, MI.

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http://dx.doi.org/10.2217/fnl.13.61DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5568855PMC
January 2014
9 Reads

Unlocking truths of γ-secretase in Alzheimer's disease: what is the translational potential?

Authors:
Michael S Wolfe

Future Neurol 2014;9(4):419-429

Center for Neurologic Disease, Brigham & Women's Hospital, Harvard Medical School, Boston, MA 02115, USA; Tel.: +1 617 525 5511;

Considerable evidence, particularly from genetics, points to the aggregation-prone amyloid β-peptide as a pathogenic entity in Alzheimer's disease. Hence, the proteases that produce this peptide from its precursor protein have been prime targets for the development of potential therapeutics. One of these proteases, γ-secretase, has been a particular focus. Read More

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http://dx.doi.org/10.2217/fnl.14.35DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4486289PMC
January 2014
15 Reads

Recent Progress in Rett Syndrome and MeCP2 Dysfunction: Assessment of Potential Treatment Options.

Future Neurol 2013 Jan;8(1)

Department of Neurobiology, Civitan International Research Center, The University of Alabama at Birmingham, Birmingham, AL 35294, USA ; Department of Pediatrics, Civitan International Research Center, The University of Alabama at Birmingham, Birmingham, AL 35294, USA.

Synaptic communication is highly regulated process of contact between cells allowing information to be stored and modified. Synaptic formation and maturation is the result of interactions between intrinsic genetic/molecular factors and the external environment to establish the communication in the brain. One disorder associated with faulty synapse communication is Rett Syndrome (RTT). Read More

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http://dx.doi.org/10.2217/fnl.12.79DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3859379PMC
January 2013
8 Reads

Therapy development for neuromuscular diseases: translating hope into promise.

Authors:
Carmen Bertoni

Future Neurol 2013 Jul;8(4)

Department of Neurology, David Geffen School of Medicine, University of California Los Angeles, 710 Westwood Plaza, Los Angeles, CA 90095, USA.

The Second Muscular Dystrophy Association Scientific Meeting was held on 21-24 April 2013 in Washington (DC, USA). The meeting provided an opportunity for research scientists, clinicians, government agencies and industry experts to highlight and discuss different aspects of therapy development for neuromuscular diseases, including novel targets, biomarkers, therapeutic approaches, animal models and clinical trials. With 500 participants, 66 presentations and 200 abstracts, the 3-day conference has become a central focus for scientists interested in translational research and moving potential therapies forward from the bench to the bedside. Read More

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http://dx.doi.org/10.2217/fnl.13.29DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3834955PMC
July 2013
3 Reads

Understanding the neurobiology of CD200 and the CD200 receptor: a therapeutic target for controlling inflammation in human brains?

Future Neurol 2013 May;8(3)

Laboratory of Neuroinflammation, Banner Sun Health Research Institute, 10515 West Santa Fe Drive, Sun City, AZ 85351, USA.

CD200 and its receptor, CD200 receptor (CD200R), have uniaue roles in controlling damaging inflammatory processes. At present, the only identified function for CD200 is as a ligand for CD200R. These proteins interact resulting in the activation of anti-inflammatory signaling by CD200R-expressing cells. Read More

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http://dx.doi.org/10.2217/fnl.13.14DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3815586PMC
May 2013
5 Reads

Advances in the treatment of visual hallucinations in neurodegenerative diseases.

Future Neurol 2013 Jul;8(4):433-444

Northumberland, Tyne & Wear NHS Foundation Trust & Newcastle University, Bensham Hospital, Gateshead, NE8 4YL, UK.

Treatment of visual hallucinations in neurodegenerative disorders is not well advanced. The complexity of underlying mechanisms presents a number of potential avenues for developing treatments, but also suggests that any single one may be of limited efficacy. Reducing medication, with the careful introduction of antidementia medication if needed, is the mainstay of current management. Read More

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http://dx.doi.org/10.2217/fnl.13.19DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3717328PMC
July 2013
18 Reads

Astroglia in neurological diseases.

Future Neurol 2013 Mar;8(2):149-158

Faculty of Life Sciences, The University of Manchester, Manchester, UK ; Ikerbasque, Basque Foundation for Science, 48011, Bilbao, Spain ; Department of Neurosciences, University of the Basque Country UPV/EHU 48940, Leioa, Spain ; Institute of Experimental Medicine, ASCR, Videnska 1083, 142 20, Prague, Czech Republic.

Astroglia encompass a subset of versatile glial cells that fulfill a major homeostatic role in the mammalian brain. Since any brain disease results from failure in brain homeostasis, astroglial cells are involved in many, if not all, aspects of neurological and/or psychiatric disorders. In this article, the roles of astrocytes as homeostatic cells in healthy and diseased brains are surveyed. Read More

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http://dx.doi.org/10.2217/fnl.12.90DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3645493PMC
March 2013
26 Reads

The expanding genomic landscape of autism: discovering the 'forest' beyond the 'trees'

Authors:
Valerie W Hu

Future Neurol 2013 Jan;8(1):29-42

Department of Biochemistry & Molecular Medicine, The George Washington University, School of Medicine & Health Sciences, 2300 Eye St., N.W., Washington, DC 20037, USA Tel.: +1 202 994 8431

Autism spectrum disorders are neurodevelopmental disorders characterized by significant deficits in reciprocal social interactions, impaired communication and restricted, repetitive behaviors. As autism spectrum disorders are among the most heritable of neuropsychiatric disorders, much of autism research has focused on the search for genetic variants in protein-coding genes (i.e. Read More

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http://dx.doi.org/10.2217/fnl.12.83DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3637978PMC
January 2013
4 Reads

mTOR as a potential treatment target for epilepsy.

Authors:
Michael Wong

Future Neurol 2012 Sep;7(5):537-545

Department of Neurology & The Hope Center for Neurological Disorders, Washington University School of Medicine, Box 8111, 660 South Euclid Avenue, St Louis, MO 63110, USA, Tel.: +1 314 362 8713, ,

Current treatments for epilepsy suffer from significant limitations, including medical intractability and lack of disease-modifying or anti-epileptogenic actions. As most current seizure medications modulate ion channels and neurotransmitter receptors, more effective therapies likely need to target completely different mechanisms of action. The mammalian target of rapamycin (mTOR) pathway represents a potential novel therapeutic target for epilepsy. Read More

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http://dx.doi.org/10.2217/fnl.12.45DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3632418PMC
September 2012
4 Reads

ADVANCES IN THE CELL-BASED TREATMENT OF NEONATAL HYPOXIC-ISCHEMIC BRAIN INJURY.

Future Neurol 2013 Mar;8(2):193-203

Department of Neurosurgery and Brain Repair, University of South Florida, College of Medicine, Tampa, Florida 33612 USA.

Stem cell therapy for adult stroke has reached limited clinical trials. Here, we provide translational research guidance on stem cell therapy for neonatal hypoxic-ischemic brain injury requiring a careful consideration of clinically relevant animal models, feasible stem cell sources, and validated safety and efficacy endpoint assays, as well as a general understanding of modes of action of this cellular therapy. To this end, we refer to existing translational guidelines, in particular the recommendations outlined in the consortium of academicians, industry partners and regulators called Stem cell Therapeutics as an Emerging Paradigm for Stroke or STEPS. Read More

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http://dx.doi.org/10.2217/fnl.12.85DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3615569PMC
March 2013
4 Reads

Persistent region-dependent neuroinflammation, NMDA receptor loss and atrophy in an animal model of penetrating brain injury.

Future Neurol 2012 May;7(3):329-339

Neurosurgery Department, Chaim Sheba Medical Center, Tel Hashomer, Israel.

Dynamic changes in neuroinflammation and glutamate NMDA receptors (NMDAR) have been noted in traumatic and ischemic brain injury.

Aim: Here we investigate the time course and regional distribution of these changes and their relationship with atrophy in a rat model of penetrating brain injury.

Materials Methods: Quantitative autoradiography, with the neuroinflammation marker [H]PK11195 and the NMDAR antagonist [I]iodoMK801, was performed on brains of animals subjected to a unilateral wireknife injury at the level of striatum and killed 3 - 60 days later. Read More

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http://dx.doi.org/10.2217/fnl.12.25DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3607550PMC
May 2012
10 Reads

Malignant synaptic growth and Alzheimer's disease.

Future Neurol 2012 Sep;7(5):557-571

Center for Memory & Brain, Boston University, 2 Cummington St, Boston, MA 02215, USA.

In this article, we will describe the malignant synaptic growth hypothesis of Alzheimer's disease. Originally presented in 1994, the hypothesis remains a viable model of the functional and biophysical mechanisms underlying the development and progression of Alzheimer's disease. In this article, we will refresh the model with references to relevant empirical support that has been generated in the intervening two decades since it's original presentation. Read More

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http://dx.doi.org/10.2217/fnl.12.47DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3571723PMC
September 2012
5 Reads

Aging of the NMDA receptor: from a mouse's point of view.

Future Neurol 2012 Sep;7(5):627-637

Department of Biomedical Sciences, College of Veterinary Medicine, Healthy Aging Program, Linus Pauling Institute, Oregon State University, Corvallis, OR 97331, USA ■ Tel.: +1 541 737 6923 ■ ■

Our elderly population is growing and declines in cognitive abilities, such as memory, can be costly, because it can interfere with a person's ability to live independently. The NMDA receptor is very important for many different forms of memory and this receptor is negatively affected by aging. This review examines the progress that has been made recently in characterizing selective vulnerabilities of different subunits and splice variants of the NMDA receptor to normal aging in C57BL/6 mice. Read More

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http://dx.doi.org/10.2217/fnl.12.54DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3540203PMC
September 2012
19 Reads

Opening Pandora's jar: a primer on the putative roles of CRMP2 in a panoply of neurodegenerative, sensory and motor neuron, and central disorders.

Future Neurol 2012 Nov;7(6):749-771

Program in Medical Neurosciences, Paul & Carole Stark Neurosciences Research Institute Indianapolis, IN 46202, USA ; Departments of Pharmacology & Toxicology, Indianapolis, IN 46202, USA ; Biochemistry & Molecular Biology, Indiana University School of Medicine, Indianapolis, IN 46202, USA ; Sophia Therapeutics LLC, Indianapolis, IN 46202, USA.

CRMP2, also known as DPYSL2/DRP2, Unc-33, Ulip or TUC2, is a cytosolic phosphoprotein that mediates axon/dendrite specification and axonal growth. Mapping the CRMP2 interactome has revealed previously unappreciated functions subserved by this protein. Together with its canonical roles in neurite growth and retraction and kinesin-dependent axonal transport, it is now known that CRMP2 interacts with numerous binding partners to affect microtubule dynamics; protein endocytosis and vesicular cycling, synaptic assembly, calcium channel regulation and neurotransmitter release. Read More

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http://dx.doi.org/10.2217/FNL.12.68DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3539824PMC
November 2012
4 Reads
20 Citations

Optimizing mouse models of neurodegenerative disorders: are therapeutics in sight?

Future Neurol 2013 16;9(1):67-75. Epub 2013 Dec 16.

The Jackson Laboratory, Genetic Resource Sciences, 600 Main Street, Bar Harbor, ME 04609, USA.

The genomic and biologic conservation between mice and humans, along with our increasing ability to manipulate the mouse genome, places the mouse as a premier model for deciphering disease mechanisms and testing potential new therapies. Despite these advantages, mouse models of neurodegenerative disease are sometimes difficult to generate and can present challenges that must be carefully addressed when used for preclinical studies. For those models that do exist, the standardization and optimization of the models is a critical step in ensuring success in both basic research and preclinical use. Read More

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http://dx.doi.org/10.2217/fnl.13.66DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5822737PMC
December 2013
2 Reads

Alleviating brain stress: what alternative animal models have revealed about therapeutic targets for hypoxia and anoxia.

Future Neurol 2013 ;8(3):287-301

Department of Biological Sciences, Florida Atlantic University, 777 Glades Road, Boca Raton, FL 33431, USA.

While the mammalian brain is highly dependent on oxygen, and can withstand only a few minutes without air, there are both vertebrate and invertebrate examples of anoxia tolerance. One example is the freshwater turtle, which can withstand days without oxygen, thus providing a vertebrate model with which to examine the physiology of anoxia tolerance without the pathology seen in mammalian ischemia/reperfusion studies. Insect models such as have additional advantages, such as short lifespans, low cost and well-described genetics. Read More

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http://dx.doi.org/10.2217/fnl.13.12DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4174394PMC
January 2013
6 Reads

The role of intracellular trafficking and the VPS10d receptors in Alzheimer's disease.

Authors:
Christiane Reitz

Future Neurol 2012 Jul;7(4):423-431

The Taub Institute for Research on Alzheimer's Disease & the Aging Brain, The Gertrude H. Sergievsky Center, Columbia University, 630 W 168th Street, New York, NY 10032, USA ; The Department of Neurology, College of Physicians & Surgeons, Columbia University, 630 W 168th Street, New York, NY 10032, USA.

In Alzheimer's disease, the key pathological culprit is the amyloid-β protein, which is generated through β- and γ-secretase cleavage of the amyloid-β precursor protein (APP). Both the secretases and amyloid-β precursor protein are transmembrane proteins that are sorted via the trans-Golgi network and the endosome through multiple membranous compartments of the cell. The coat complex clathrin controls the sorting from the cell surface and the trans-Golgi network to the endosome. Read More

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http://dx.doi.org/10.2217/fnl.12.31DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3524993PMC
July 2012
5 Reads

A Critical Kinase Cascade in Neurological Disorders: PI 3-K, Akt, and mTOR.

Future Neurol 2012 Nov;7(6):733-748

Laboratory of Cellular and Molecular Signaling, Newark, New Jersey 07101 ; New Jersey Health Sciences University, Newark, New Jersey 07101.

Neurodegenerative disorders lead to disability and death in a significant proportion of the world's population. However, many disorders of the nervous system remain with limited effective treatments. Kinase pathways in the nervous system that involve phosphoinositide 3-kinase (PI 3-K), protein kinase B (Akt), and the mammalian target of rapamycin (mTOR) offer exciting prospects for the understanding of neurodegenerative pathways and the development of new avenues of treatment. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3491909PMC
November 2012
6 Reads

Molecular neuropathogenesis of Alzheimer's disease: an interaction model stressing the central role of oxidative stress.

Future Neurol 2012 May;7(3):287-305

Ave. Icaraí Cristal 74 (Clinic), 90.810-000 Porto Alegre, Rio Grande do Sul (RS), Brazil.

Alzheimer's disease (AD) exhibits a complex etiology that simultaneously manifests as a complex cellular, neurobiological, molecular, anatomic-physiological and clinical entity. Other significant psychiatric conditions, such as depression and schizophrenia, may also present with complex and concurrent clinical and/or molecular phenotypes. These neuropsychiatric pathologies also originate from both environmental and genetic factors. Read More

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http://dx.doi.org/10.2217/fnl.12.27DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3475420PMC
May 2012
11 Reads