3,149 results match your criteria Molecular and Cellular Neuroscience [Journal]


Klotho deficiency affects the spine morphology and network synchronization of neurons.

Mol Cell Neurosci 2019 Apr 13;98:1-11. Epub 2019 Apr 13.

Department of Neurobiology, University of Alabama at Birmingham, 1825 University Blvd. Shelby 913, Birmingham 35294, AL, USA. Electronic address:

Klotho-deficient mice rapidly develop cognitive impairment and show some evidence of the onset of neurodegeneration. However, it is impossible to investigate the long-term consequences on the brain because of the dramatic shortening of lifespan caused by systemic klotho deficiency. As klotho expression is downregulated with advancing organismal age, understanding the mechanisms of klotho action is important for developing novel strategies to support healthy brain aging. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S10447431183038
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http://dx.doi.org/10.1016/j.mcn.2019.04.002DOI Listing
April 2019
5 Reads

An FTLD-associated SQSTM1 variant impacts Nrf2 and NF-κB signalling and is associated with reduced phosphorylation of p62.

Mol Cell Neurosci 2019 Apr 4. Epub 2019 Apr 4.

Harry Perkins Institute of Medical Research, University of Western Australia, Nedlands, Western Australia, Australia; Department of Endocrinology and Diabetes, Sir Charles Gairdner Hospital, Nedlands, Western Australia, Australia. Electronic address:

Elevated oxidative stress has been implicated in the pathogenesis of amyotrophic lateral sclerosis (ALS) and Frontotemporal Lobar Degeneration (FTLD). In response to oxidative stress, the Nrf2 transcription factor activates protective antioxidant genes. A critical regulator of Nrf2 is the inhibitory protein Keap1, which mediates Nrf2 degradation. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S10447431183036
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http://dx.doi.org/10.1016/j.mcn.2019.04.001DOI Listing
April 2019
5 Reads

Small molecules as therapeutic drugs for Alzheimer's disease.

Mol Cell Neurosci 2019 Apr 12;96:47-62. Epub 2019 Mar 12.

Internal Medicine Department, Texas Tech University Health Sciences Center, 3601 4th Street, Lubbock, TX 79430, United State; Garrison Institute on Aging, South West Campus, Texas Tech University Health Sciences Center, 6630 S. Quaker Suite E, Lubbock, TX 79413, United States; Cell Biology & Biochemistry Department, Texas Tech University Health Sciences Center, 3601 4th Street, Lubbock, TX 79430, United States; Pharmacology & Neuroscience Department, Texas Tech University Health Sciences Center, 3601 4th Street, Lubbock, TX 79430, United States; Neurology Department, Texas Tech University Health Sciences Center, 3601 4th Street, Lubbock, TX 79430, United States; Speech, Language and Hearing Sciences Department, Texas Tech University Health Sciences Center, 3601 4th Street, Lubbock, TX 79430, United States; Department of Public Health, Graduate School of Biomedical Sciences, 3601 4th Street, Lubbock, TX 79430, United States. Electronic address:

Mitochondrial dysfunction is a central protagonist of Alzheimer's disease (AD) pathogenesis. Mitochondrial dysfunction stems from various factors including mitochondrial DNA damage and oxidative stress from reactive oxygen species, membrane and ionic gradient destabilization, and interaction with toxic proteins such as amyloid beta (Aβ). Therapeutic drugs such as cholinesterase and glutamate inhibitors have proven to improve synaptic neurotransmitters, but do not address mitochondrial dysfunction. Read More

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http://dx.doi.org/10.1016/j.mcn.2019.03.001DOI Listing
April 2019
2 Reads

Modulation of Ca2.3 channels by unconjugated bilirubin (UCB) - Candidate mechanism for UCB-induced neuromodulation and neurotoxicity.

Mol Cell Neurosci 2019 Apr 12;96:35-46. Epub 2019 Mar 12.

Institute for Neurophysiology, University of Cologne, Germany. Electronic address:

Elevated levels of unbound unconjugated bilirubin (UCB) can lead to bilirubin encephalopathy and kernicterus. In spite of a large number of studies demonstrating UCB-induced changes in central neurotransmission, it is still unclear whether these effects involve alterations in the function of specific ion channels. To assess how different UCB concentrations and UCB:albumin (U/A) molar ratios affect neuronal R-type voltage-gated Ca channels, we evaluated their effects on whole-cell currents through recombinant Ca2. Read More

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http://dx.doi.org/10.1016/j.mcn.2019.03.003DOI Listing
April 2019
1 Read
3.840 Impact Factor

Growth and excitability at synapsin II deficient hippocampal neurons.

Mol Cell Neurosci 2019 Apr 9;96:25-34. Epub 2019 Mar 9.

Department of Neurology, Wayne State University School of Medicine, Detroit, MI, United States of America. Electronic address:

Synapsins are neuronal phosphoproteins that fine-tune synaptic transmission and suppress seizure activity. Synapsin II (SynII) deletion produces epileptic seizures and overexcitability in neuronal networks. Early studies in primary neuronal cultures have shown that SynII deletion results in a delay in synapse formation. Read More

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http://dx.doi.org/10.1016/j.mcn.2019.03.002DOI Listing

Fluid and imaging biomarkers for Huntington's disease.

Mol Cell Neurosci 2019 Feb 23. Epub 2019 Feb 23.

Huntington's Disease Centre, University College London (UCL) Institute of Neurology, London WC1N 3BG, United Kingdom. Electronic address:

Huntington's disease is a chronic progressive neurodegenerative condition for which there is no disease-modifying treatment. The known genetic cause of Huntington's disease makes it possible to identify individuals destined to develop the disease and instigate treatments before the onset of symptoms. Multiple trials are already underway that target the cause of HD, yet clinical measures are often insensitive to change over typical clinical trial duration. Read More

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http://dx.doi.org/10.1016/j.mcn.2019.02.004DOI Listing
February 2019

Synaptic vesicle protein 2A as a potential biomarker in synaptopathies.

Mol Cell Neurosci 2019 Feb 20. Epub 2019 Feb 20.

Wallenberg Centre for Molecular and Translational Medicine, Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Sweden; Clinical Memory Research Unit, Lund University, Sweden; Department of Neurodegenerative Disease, UCL Institute of Neurology, Queen Square, London, UK.

Measuring synaptic density in vivo using positron emission tomography (PET) imaging-based biomarkers targeting the synaptic vesicle protein 2A (SV2A) has received much attention recently due to its potential research and clinical applications in synaptopathies, including neurodegenerative and psychiatric diseases. Fluid-based biomarkers in proteinopathies have previously been suggested to provide information on pathology and disease status that is complementary to PET-based measures, and the same can be hypothesized with respect to SV2A. This review provides an overview of the current state of SV2A PET imaging as a biomarker of synaptic density, the potential role of fluid-based biomarkers for SV2A, and related future perspectives. Read More

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http://dx.doi.org/10.1016/j.mcn.2019.02.001DOI Listing
February 2019
3.840 Impact Factor

Taxifolin protects neurons against ischemic injury in vitro via the activation of antioxidant systems and signal transduction pathways of GABAergic neurons.

Mol Cell Neurosci 2019 Apr 15;96:10-24. Epub 2019 Feb 15.

Institute of Cell Biophysics, Federal Research Center "Pushchino Scientific Center for Biological Research of the Russian Academy of Sciences", Russian Academy of Sciences, Russia. Electronic address:

Cerebral blood flow disturbances lead to the massive death of brain cells. The death of >80% of cells is observed in hippocampal cell cultures after 40 min of oxygen and glucose deprivation (ischemia-like conditions, OGD). However, there are some populations of GABAergic neurons which are characterized by increased vulnerability to oxygen-glucose deprivation conditions. Read More

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http://dx.doi.org/10.1016/j.mcn.2019.01.005DOI Listing

Neurotoxic effects of MPTP on mouse cerebral cortex: Modulation of neuroinflammation as a neuroprotective strategy.

Mol Cell Neurosci 2019 Apr 13;96:1-9. Epub 2019 Feb 13.

Research Institute for Medicines (iMed.ULisboa), Faculty of Pharmacy, Universidade de Lisboa, Av. Prof. Gama Pinto, 1649-003 Lisbon, Portugal; UCIBIO, Departamento Ciências da Vida, Faculdade de Ciências e Tecnologia, Universidade NOVA de Lisbon, Caparica, Portugal. Electronic address:

Parkinson's disease (PD) is a progressive neurological disorder, mainly characterized by the progressive loss of dopaminergic neurons in the Substantia nigra pars compacta (SNpc) and by the presence of intracellular inclusions, known as Lewy bodies. Despite SNpc being considered the primary affected region in PD, the neuropathological features are confined solely to the nigro-striatal axis. With disease progression other brain regions are also affected, namely the cerebral cortex, although the spreading of the neurologic damage to this region is still not completely unraveled. Read More

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http://dx.doi.org/10.1016/j.mcn.2019.01.003DOI Listing
April 2019
1 Read
3.840 Impact Factor

Sympathomimetics regulate neuromuscular junction transmission through TRPV1, P/Q- and N-type Ca channels.

Mol Cell Neurosci 2019 03 11;95:59-70. Epub 2019 Feb 11.

Department of Internal Medicine, Section on Gerontology and Geriatric Medicine, Wake Forest School of Medicine, Winston-Salem, NC, United States of America; Neuroscience Program, Wake Forest School of Medicine, Winston-Salem, NC, United States of America. Electronic address:

Increasing evidence indicates that, first, the sympathetic nervous system interacts extensively with both vasculature and skeletal muscle fibers near neuromuscular junctions (NMJs) and, second, its neurotransmitter, noradrenaline, influences myofiber molecular composition and function and motor innervation. Since sympathomimetic agents have been reported to improve NMJ transmission, we examined whether two in clinical use, salbutamol and clenbuterol, affect the motor axon terminal via extracellular Ca and molecular targets, such as TRPV1 and P/Q- and N-type voltage-activated Ca channels. Electrophysiological recordings in ex-vivo preparations of peroneal nerves and lumbricalis muscles from young adult mice focused on spontaneous miniature end-plate potentials and singly and repetitively evoked end-plate potentials. Read More

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http://dx.doi.org/10.1016/j.mcn.2019.01.007DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6394868PMC

CPEB1 is overexpressed in neurons derived from Down syndrome IPSCs and in the hippocampus of the mouse model Ts1Cje.

Mol Cell Neurosci 2019 03 11;95:79-85. Epub 2019 Feb 11.

Departamento de Fisiología Médica y Biofísica, Universidad de Sevilla, Sevilla, Spain; Instituto de Biomedicina de Sevilla, IBIS/Hospital Universitario Virgen del Rocío/CSIC/Universidad de Sevilla, Sevilla, Spain. Electronic address:

Trisomy 21, also known as Down syndrome (DS), is the most frequent genetic cause of intellectual impairment. In mouse models of DS, deficits in hippocampal synaptic plasticity have been observed, in conjunction with alterations to local dendritic translation that are likely to influence plasticity, learning and memory. Here we show that expression of a local translational regulator, the Cytoplasmic Polyadenylation Element Binding Protein 1 (CPEB1), is enhanced in hippocampal neurons from the Ts1Cje DS mouse model. Read More

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http://dx.doi.org/10.1016/j.mcn.2019.02.002DOI Listing
March 2019
2 Reads

APP depletion alters selective pre- and post-synaptic proteins.

Mol Cell Neurosci 2019 03 11;95:86-95. Epub 2019 Feb 11.

Experimental Dementia Research Unit, Department of Experimental Medical Science, Lund University, Lund, Sweden; Department of Neurology and Neuroscience, Weill Cornell Medical College, New York, NY, USA. Electronic address:

The normal role of Alzheimer's disease (AD)-linked amyloid precursor protein (APP) in the brain remains incompletely understood. Previous studies have reported that lack of APP has detrimental effects on spines and electrophysiological parameters. APP has been described to be important in synaptic pruning during development. Read More

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http://dx.doi.org/10.1016/j.mcn.2019.02.003DOI Listing
March 2019
2 Reads
3.840 Impact Factor

Interleukin-16 inhibits sodium channel function and GluA1 phosphorylation via CD4- and CD9-independent mechanisms to reduce hippocampal neuronal excitability and synaptic activity.

Mol Cell Neurosci 2019 03 7;95:71-78. Epub 2019 Feb 7.

Strathclyde Institute of Pharmacy and Biomedical Sciences, University of Strathclyde, 161 Cathedral Street, Glasgow G4 0RE, UK. Electronic address:

Interleukin 16 (IL-16) is a cytokine that is primarily associated with CD4 T cell function, but also exists as a multi-domain PDZ protein expressed within cerebellar and hippocampal neurons. We have previously shown that lymphocyte-derived IL-16 is neuroprotective against excitotoxicity, but evidence of how it affects neuronal function is limited. Here, we have investigated whether IL-16 modulates neuronal excitability and synaptic activity in mouse primary hippocampal cultures. Read More

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http://dx.doi.org/10.1016/j.mcn.2019.01.002DOI Listing

Stem cells in animal models of Huntington disease: A systematic review.

Mol Cell Neurosci 2019 03 24;95:43-50. Epub 2019 Jan 24.

Neuropsychiatry Program, Department of Psychiatry and Behavioral Sciences, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX, USA.

Huntington's disease (HD) is an autosomal-dominant neurodegenerative disorder encoding a mutant form of the huntingtin protein (HTT). HD is pathologically characterized by loss of neurons in the striatum and cortex, which leads to progressive motor dysfunction, cognitive decline and behavioral symptoms. Stem cell-based therapy has emerged as a feasible therapeutic approach for the treatment of neurodegenerative diseases and may be effective in alleviating and/or halting the pathophysiological mechanisms underlying HD. Read More

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http://dx.doi.org/10.1016/j.mcn.2019.01.006DOI Listing
March 2019
2 Reads

Norepinephrine control of ventromedial hypothalamic nucleus glucoregulatory neurotransmitter expression in the female rat: Role of monocarboxylate transporter function.

Mol Cell Neurosci 2019 03 17;95:51-58. Epub 2019 Jan 17.

School of Basic Pharmaceutical and Toxicological Sciences, College of Pharmacy, University of Louisiana Monroe, Monroe, LA 71201, United States of America. Electronic address:

The ventromedial hypothalamic nucleus (VMN) is a critical component of the neural circuitry that regulates glucostasis. Astrocyte glycogen is a vital reserve of glucose and its oxidizable metabolite L-lactate. In hypoglycemic female rats, estradiol-dependent augmentation of VMN glycogen phosphorylase (GP) protein requires hindbrain catecholamine input. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S10447431183030
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http://dx.doi.org/10.1016/j.mcn.2019.01.004DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6472905PMC
March 2019
2 Reads

siRNA-mediated knockdown of B3GALT4 decreases GM1 ganglioside expression and enhances vulnerability for neurodegeneration.

Mol Cell Neurosci 2019 03 3;95:25-30. Epub 2019 Jan 3.

Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, PA 19107, United States of America. Electronic address:

Reduced levels of brain gangliosides GD1a, GD1b, GT1b and to a lesser extent GM1 have been found in substantia nigra (SN) from Parkinson's disease (PD) patients, along with decreased gene expression for key enzymes (B3Galt4, St3gal2) involved in synthesis of these gangliosides. Based on these observations, the present study examined the extent to which decreased expression of B3GALT4 mRNA and resulting decreased levels of GM1 ganglioside in dopaminergic cells may increase the vulnerability of these cells to degeneration in response to a neurotoxicant exposure that under normal circumstances would not result in neurodegeneration. Differentiated SK-N-SH cells were treated with B3GALT4 siRNA to significantly reduce B3GALT4 mRNA expression and decrease GM1 levels. Read More

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http://dx.doi.org/10.1016/j.mcn.2019.01.001DOI Listing

Alteration of parvalbumin expression and perineuronal nets formation in the cerebral cortex of aged mice.

Mol Cell Neurosci 2019 03 2;95:31-42. Epub 2019 Jan 2.

Department of Psychiatry, Kawasaki Medical School, Kurashiki 701-0192, Japan. Electronic address:

Aging is associated with decline in cognitive function, but the underlying mechanisms have not been elucidated. Normal activity of pyramidal cells and parvalbumin-expressing interneurons (PV neurons) is essential for cognitive function. PV neurons participate in the regulation of pyramidal-cell firing. Read More

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http://dx.doi.org/10.1016/j.mcn.2018.12.008DOI Listing

Ouabain activates transcription factor EB and exerts neuroprotection in models of Alzheimer's disease.

Mol Cell Neurosci 2019 03 28;95:13-24. Epub 2018 Dec 28.

Department of Brain Science, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea; Bio-Medical Institute of Technology (BMIT), University of Ulsan College of Medicine, Seoul, Republic of Korea; Institute for Innovation in Neurodegenerative Diseases, ADEL, Inc., Seoul, Republic of Korea. Electronic address:

The number of neurofibrillary tangles containing abnormal hyperphosphorylated tau protein correlates with the degree of dementia in Alzheimer's disease (AD). In addition, autophagosome accumulation and disturbance of autophagy, the process by which toxic aggregate proteins are degraded in the cytosol, are also found in AD models. These indicate that regulation of the autophagy-lysosome system may be a potential therapeutic target for AD. Read More

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http://dx.doi.org/10.1016/j.mcn.2018.12.007DOI Listing

Impairment of chaperone-mediated autophagy affects neuronal homeostasis through altered expression of DJ-1 and CRMP-2 proteins.

Mol Cell Neurosci 2019 03 15;95:1-12. Epub 2018 Dec 15.

Center of Clinical Research, Experimental Surgery and Translational Research, Biomedical Research Foundation, Academy of Athens, Athens, Greece; Second Department of Neurology, National and Kapodistrian University of Athens Medical School, Athens, Greece. Electronic address:

Chaperone-mediated autophagy (CMA) is a substrate-specific mode of lysosomal proteolysis, with multiple lines of evidence connecting its dysfunction to both ageing and disease. We have recently shown that CMA impairment through knock-down of the lysosomal receptor LAMP2A is detrimental to neuronal viability in vivo; however, it is not clear which subset of proteins regulated by the CMA pathway mediate such changes. In this study, we have manipulated CMA function through alterations of LAMP2A abundance in primary rat cortical neurons, to identify potential changes to the neuronal proteome occurring prior to neurotoxic effects. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S10447431183018
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http://dx.doi.org/10.1016/j.mcn.2018.12.006DOI Listing
March 2019
8 Reads

Cerebrospinal fluid biomarker for Parkinson's disease: An overview.

Mol Cell Neurosci 2018 Dec 10. Epub 2018 Dec 10.

University Medical Center, Department of Neurology, Robert-Koch Strasse 40, 37075 Goettingen, Germany.

In Parkinson's disease (PD), there is a wide field of recent and ongoing search for useful biomarkers for early and differential diagnosis, disease monitoring or subtype characterization. Up to now, no biofluid biomarker has entered the daily clinical routine. Cerebrospinal fluid (CSF) is often used as a source for biomarker development in different neurological disorders because it reflects changes in central-nervous system homeostasis. Read More

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http://dx.doi.org/10.1016/j.mcn.2018.12.005DOI Listing
December 2018
1 Read

Fluid and PET biomarkers for amyloid pathology in Alzheimer's disease.

Mol Cell Neurosci 2018 Dec 8. Epub 2018 Dec 8.

Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Molndal, Sweden; Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, University College, London, United Kingdom of Great Britain and Northern Ireland; Department of Molecular Neuroscience, UCL Institute of Neurology, United Kingdom of Great Britain and Northern Ireland; UK Dementia Research Institute at UCL, United Kingdom of Great Britain and Northern Ireland.

Alzheimer's disease (AD) is characterized by amyloid plaques and tau pathology (neurofibrillary tangles and neuropil threads). Amyloid plaques are primarily composed of aggregated and oligomeric β-amyloid (Aβ) peptides ending at position 42 (Aβ42). The development of fluid and PET biomarkers for Alzheimer's disease (AD), has allowed for detection of Aβ pathology in vivo and marks a major advancement in understanding the role of Aβ in Alzheimer's disease (AD). Read More

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http://dx.doi.org/10.1016/j.mcn.2018.12.004DOI Listing
December 2018
18 Reads

Biomarkers for tau pathology.

Mol Cell Neurosci 2018 Dec 7. Epub 2018 Dec 7.

Helen Wills Neuroscience Institute, University of California, Berkeley, USA; Molecular Biophysics and Integrated Bioimaging, Lawrence Berkeley National Laboratory, Berkeley, CA, USA.

The aggregation of fibrils of hyperphosphorylated and C-terminally truncated microtubule-associated tau protein characterizes 80% of all dementia disorders, the most common neurodegenerative disorders. These so-called tauopathies are hitherto not curable and their diagnosis, especially at early disease stages, has traditionally proven difficult. A keystone in the diagnosis of tauopathies was the development of methods to assess levels of tau protein in vivo in cerebrospinal fluid, which has significantly improved our knowledge about these conditions. Read More

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http://dx.doi.org/10.1016/j.mcn.2018.12.001DOI Listing
December 2018
2 Reads

Melanocortin 4 receptor activation protects striatal neurons and glial cells from 3-nitropropionic acid toxicity.

Mol Cell Neurosci 2019 01 4;94:41-51. Epub 2018 Dec 4.

Instituto de Investigaciones Biomédicas (INBIOMED) UBA-CONICET, Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina. Electronic address:

α-Melanocyte stimulating hormone (α-MSH) is a melanocortin which exerts potent anti-inflammatory and anti-apoptotic effects. Melanocortin 4 receptors (MC4R) are abundantly expressed in the brain and we previously demonstrated that [Nle(4), D-Phe(7)]melanocyte-stimulating hormone (NDP-MSH), an α-MSH analogue, increased expression of brain derived-neurotrophic factor (BDNF), and peroxisome proliferator-activated receptor-γ (PPAR-γ). We hypothesized that melanocortins could affect striatal cell survival through BDNF and PPAR-γ. Read More

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http://dx.doi.org/10.1016/j.mcn.2018.12.002DOI Listing
January 2019

Review: Fluid biomarkers in the human prion diseases.

Mol Cell Neurosci 2018 Dec 4. Epub 2018 Dec 4.

MRC Prion Unit at University College London (UCL), UCL Institute of Prion Diseases, UCL, London W1W 7FF, United Kingdom of Great Britain and Northern Ireland. Electronic address:

The human prion diseases are a diverse set of often rapidly progressive neurodegenerative conditions associated with abnormal forms of the prion protein. We review work to establish diagnostic biomarkers and assays that might fill other important roles, particularly those that could assist the planning and interpretation of clinical trials. The field now benefits from highly sensitive and specific diagnostic biomarkers using cerebrospinal fluid: detecting by-products of rapid neurodegeneration or specific functional properties of abnormal prion protein, with the second generation real time quaking induced conversion (RT-QuIC) assay being particularly promising. Read More

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http://dx.doi.org/10.1016/j.mcn.2018.12.003DOI Listing
December 2018

Cyclo(His-Pro) inhibits NLRP3 inflammasome cascade in ALS microglial cells.

Mol Cell Neurosci 2019 01 13;94:23-31. Epub 2018 Nov 13.

Department of Experimental Medicine, University of Perugia, Perugia, Italy. Electronic address:

Neuroinflammation, i.e. self-propelling progressive cycle of microglial activation and neuron damage, as well as improper protein folding, are recognized as major culprits of neurodegenerative diseases, such as amyotrophic lateral sclerosis (ALS). Read More

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https://linkinghub.elsevier.com/retrieve/pii/S10447431183024
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http://dx.doi.org/10.1016/j.mcn.2018.11.002DOI Listing
January 2019
13 Reads

Interaction of nectin-2α with the auxiliary protein of the voltage-gated A-type K channel Kv4.2 dipeptidyl aminopeptidase-like protein at the boundary between the adjacent somata of clustered cholinergic neurons in the medial habenula.

Mol Cell Neurosci 2019 01 5;94:32-40. Epub 2018 Nov 5.

Division of Pathogenetic Signaling, Department of Biochemistry and Molecular Biology, Kobe University Graduate School of Medicine, Kobe, Hyogo 650-0047, Japan. Electronic address:

The medial habenula (MHb) receives septal inputs and sends efferents to the interpeduncular nucleus and is implicated in stress, depression, memory, and nicotine withdrawal syndrome. We previously showed by immunofluorescence microscopy that the cell adhesion molecule nectin-2α is expressed in the cholinergic neurons in the developing and adult mouse MHbs and localized at the boundary between the adjacent somata of clustered cholinergic neurons where the voltage-gated A-type K channel Kv4.2 is localized. Read More

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http://dx.doi.org/10.1016/j.mcn.2018.11.001DOI Listing
January 2019
2 Reads

Strain differences in hippocampal synaptic dysfunction in the TgCRND8 mouse model of Alzheimer's disease: Implications for improving translational capacity.

Mol Cell Neurosci 2019 01 4;94:11-22. Epub 2018 Nov 4.

Division of Neurodegenerative Disorders, St. Boniface Hospital Albrechtsen Research Centre, Winnipeg, MB, Canada R2H 2A6; Department of Pharmacology & Therapeutics, University of Manitoba, Winnipeg, Manitoba, Canada R3E 0W3. Electronic address:

In Alzheimer's disease (AD), characterized by cognitive deterioration, synaptic alterations are frequently reported. The TgCRND8 model, in which mice develop AD-like amyloid β plaque formation, has been used to investigate the effects of amyloidosis on synaptic function. Background strain impacts the behavioral and neuropathological phenotype of mice in this model, but whether this extends to synaptic function is unknown. Read More

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http://dx.doi.org/10.1016/j.mcn.2018.10.005DOI Listing
January 2019
3 Reads

Biomarkers for diseases with TDP-43 pathology.

Mol Cell Neurosci 2018 Nov 3. Epub 2018 Nov 3.

Department of Neurology, University of Ulm, Ulm, Germany. Electronic address:

The discovery that aggregated transactive response DNA-binding protein 43 kDa (TDP-43) is the major component of pathological ubiquitinated inclusions in amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD) caused seminal progress in the unveiling of the genetic bases and molecular characteristics of these now so-called TDP-43 proteinopathies. Substantial increase in the knowledge of clinic-pathological coherencies, especially for FTLD variants, could be made in the last decade, but also revealed a considerable complexity of TDP-43 pathology and often a poor correlation of clinical and molecular disease characteristics. To date, an underlying TDP-43 pathology can be predicted only for patients with mutations in the genes C9orf72 and GRN, but is dependent on neuropathological verification in patients without family history, which represent the majority of cases. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S10447431183031
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http://dx.doi.org/10.1016/j.mcn.2018.10.003DOI Listing
November 2018
12 Reads

A new function for Prokineticin 2: Recruitment of SVZ-derived neuroblasts to the injured cortex in a mouse model of traumatic brain injury.

Mol Cell Neurosci 2019 01 1;94:1-10. Epub 2018 Nov 1.

Department of Biochemistry, Laboratory of Neurobiology, Escola Paulista de Medicina, Universidade Federal de São Paulo, Rua Pedro de Toledo, 669 - 3o andar, São Paulo, SP 04039-032, Brazil. Electronic address:

Traumatic brain injury is an important cause of global morbidity and mortality. After an initial injury, there is a cascade of cellular and molecular events that ultimately lead to cell death. Therapies aim to both counteract these mechanisms and replenish the lost cell population in order to improve recovery. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S10447431183021
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http://dx.doi.org/10.1016/j.mcn.2018.10.004DOI Listing
January 2019
12 Reads

d-Cysteine promotes dendritic development in primary cultured cerebellar Purkinje cells via hydrogen sulfide production.

Mol Cell Neurosci 2018 12 19;93:36-47. Epub 2018 Oct 19.

Department of Chemico-Pharmacological Sciences, Graduate School of Pharmaceutical Sciences, Kumamoto University, Kumamoto, Japan.

Hydrogen sulfide and reactive sulfur species are regulators of physiological functions, have antioxidant effects against oxidative stresses, and are endogenously generated from l-cysteine. Recently, a novel pathway that generates hydrogen sulfide and reactive sulfur species from d-cysteine has been identified. d-Amino acid oxidase (DAO) is involved in this pathway and, among the various brain regions, is especially abundant in the cerebellum. Read More

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http://dx.doi.org/10.1016/j.mcn.2018.10.002DOI Listing
December 2018

Validation of reference genes for normalization of real-time quantitative PCR studies of gene expression in brain capillary endothelial cells cultured in vitro.

Mol Cell Neurosci 2018 12 10;93:27-35. Epub 2018 Oct 10.

Department of Pharmacy, Faculty of Health and Medical Sciences, University of Copenhagen, Universitetsparken 2, DK-2100 Copenhagen, Denmark. Electronic address:

Background: The genes encoding β-actin and GAPDH are two of the most commonly used reference genes for normalization in in vitro blood-brain barrier studies. Studies have, however, shown that these reference genes might not always be the best choice. The aim of the present study was to evaluate 10 reference genes for use in mRNA profiling studies in primary cultures of brain endothelial cells of bovine origin. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S10447431183006
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http://dx.doi.org/10.1016/j.mcn.2018.10.001DOI Listing
December 2018
1 Read

Reduced retromer function results in the accumulation of amyloid-beta oligomers.

Mol Cell Neurosci 2018 12 23;93:18-26. Epub 2018 Sep 23.

Department of Clinical Pathology and Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden. Electronic address:

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by a progressive loss of multiple cognitive functions. Accumulation of amyloid beta oligomers (oAβ) play a major role in the neurotoxicity associated with the disease process. One of the early affected brain regions is the hippocampus, wherein a reduction of the vacuolar protein sorting-associated protein 35 (VPS35), the core protein comprising the retromer complex involved in cellular cargo sorting, has been identified. Read More

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http://dx.doi.org/10.1016/j.mcn.2018.09.003DOI Listing
December 2018
1 Read

Centella asiatica attenuates hippocampal mitochondrial dysfunction and improves memory and executive function in β-amyloid overexpressing mice.

Mol Cell Neurosci 2018 12 22;93:1-9. Epub 2018 Sep 22.

Department of Neurology, Oregon Health and Science University, Portland, OR 97239, USA.

Centella asiatica is a medicinal plant used to enhance memory. We have previously shown that a water extract of Centella asiatica (CAW) attenuates β-amyloid (Aβ)-induced spatial memory deficits in mice and improves neuronal health. Yet the effect of CAW on other cognitive domains remains unexplored as does its in vivo mechanism of improving Aβ-related cognitive impairment. Read More

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http://dx.doi.org/10.1016/j.mcn.2018.09.002DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6242741PMC
December 2018
7 Reads
3.840 Impact Factor

Effects of gem-dihydroperoxides against mutant copper‑zinc superoxide dismutase-mediated neurotoxicity.

Mol Cell Neurosci 2018 10 5;92:177-184. Epub 2018 Sep 5.

Laboratory of Medical Therapeutics and Molecular Therapeutics, Gifu Pharmaceutical University, Gifu, Japan. Electronic address:

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder characterized by progressive muscle weakness, paralysis, and death. Although its neuropathology is well investigated, currently, effective treatments are unavailable. The mechanism of ALS involves the aggregation and accumulation of several mutant proteins, including mutant copper‑zinc superoxide dismutase (SOD1), TAR DNA binding protein 43 kDa (TDP-43) and fused in sarcoma (FUS) proteins. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S10447431183016
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http://dx.doi.org/10.1016/j.mcn.2018.09.001DOI Listing
October 2018
5 Reads

Membrane trafficking and cytoskeletal dynamics in neuronal function.

Mol Cell Neurosci 2018 09;91:1-2

Division of Cell Biology, Department of Biology, Faculty of Science, Utrecht University, 3584 CH, The Netherlands. Electronic address:

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http://dx.doi.org/10.1016/j.mcn.2018.08.003DOI Listing
September 2018

Deletion of Kir6.2/SUR1 potassium channels rescues diminishing of DA neurons via decreasing iron accumulation in PD.

Mol Cell Neurosci 2018 10 29;92:164-176. Epub 2018 Aug 29.

Department of Pharmacology, School of Medicine and Life Sciences, Nanjing University of Chinese Medicine, 138 Xianlin Avenue, Nanjing, Jiangsu 210023, China; Jiangsu Key Laboratory of Neurodegeneration, Department of Pharmacology, Nanjing Medical University, 101 Longmian Avenue, Nanjing, Jiangsu 211166, China. Electronic address:

ATP-sensitive potassium (K-ATP) channels express in the central nervous system extensively which coupling cell metabolism and cellular electrical activity. K-ATP channels in mature substantia nigra (SN) dopaminergic (DA) neurons are composed of inwardly rectifying potassium channel (Kir) subunit 6.2 and sulfonylurea receptor 1 (SUR1). Read More

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http://dx.doi.org/10.1016/j.mcn.2018.08.006DOI Listing
October 2018
15 Reads

Polyglutamine repeat proteins disrupt actin structure in Drosophila photoreceptors.

Mol Cell Neurosci 2018 12 24;93:10-17. Epub 2018 Aug 24.

University of San Diego, Department of Biology, 5998 Alcala Park Blvd, SCST 372, San Diego, CA 92110, USA. Electronic address:

Expansions of polygutamine-encoding stretches in several genes cause neurodegenerative disorders including Huntington's Disease and Spinocerebellar Ataxia type 3. Expression of the human disease alleles in Drosophila melanogaster neurons recapitulates cellular features of these disorders, and has therefore been used to model the cell biology of these diseases. Here, we show that polyglutamine disease alleles expressed in Drosophila photoreceptors disrupt actin structure at rhabdomeres, as other groups have shown they do in Drosophila and mammalian dendrites. Read More

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http://dx.doi.org/10.1016/j.mcn.2018.08.005DOI Listing
December 2018
17 Reads

Neural progenitors derived from Tuberous Sclerosis Complex patients exhibit attenuated PI3K/AKT signaling and delayed neuronal differentiation.

Mol Cell Neurosci 2018 10 23;92:149-163. Epub 2018 Aug 23.

Department of Cell Biology and Neuroscience, Rutgers, the State University of New Jersey, Piscataway, NJ, United States of America; Human Genetics Institute of New Jersey, Piscataway, NJ, United States of America. Electronic address:

Tuberous Sclerosis Complex (TSC) is a disease caused by autosomal dominant mutations in the TSC1 or TSC2 genes, and is characterized by tumor susceptibility, brain lesions, seizures and behavioral impairments. The TSC1 and TSC2 genes encode proteins forming a complex (TSC), which is a major regulator and suppressor of mammalian target of rapamycin complex 1 (mTORC1), a signaling complex that promotes cell growth and proliferation. TSC1/2 loss of heterozygosity (LOH) and the subsequent complete loss of TSC regulatory activity in null cells causes mTORC1 dysregulation and TSC-associated brain lesions or other tissue tumors. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S10447431183008
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http://dx.doi.org/10.1016/j.mcn.2018.08.004DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6250058PMC
October 2018
19 Reads

Defective mitochondrial and lysosomal trafficking in chorea-acanthocytosis is independent of Src-kinase signaling.

Mol Cell Neurosci 2018 10 3;92:137-148. Epub 2018 Aug 3.

Division of Neurodegenerative Diseases, Department of Neurology, Technische Universität Dresden, Dresden, Germany; Center for Regenerative Therapies Dresden (CRTD), Technische Universität Dresden, Dresden, Germany; German Center for Neurodegenerative Diseases (DZNE) Dresden, Dresden, Germany; Universitäts Centrum für seltene Erkrankungen, Technische Universität Dresden, Dresden, Germany. Electronic address:

Mutations in the VPS13A gene leading to depletion of chorein protein are causative for Chorea Acanthocytosis (ChAc), a rare devastating disease, which is characterized by neurodegeneration mainly affecting the basal ganglia as well as deformation of erythrocytes. Studies on patient blood samples highlighted a dysregulation of Actin cytoskeleton caused by downregulation of the PI3K pathway and hyper-activation of Lyn-kinase, but to what extent these mechanisms are present and relevant in the affected neurons remains elusive. We studied the effects of the absence of chorein protein on the morphology and trafficking of lysosomal and mitochondrial compartments in ChAc patient-specific induced pluripotent stem cell-derived medium spiny neurons (MSNs). Read More

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http://dx.doi.org/10.1016/j.mcn.2018.08.002DOI Listing
October 2018
3 Reads

The effect of Jun dimerization on neurite outgrowth and motif binding.

Mol Cell Neurosci 2018 10 3;92:114-127. Epub 2018 Aug 3.

Miami Project to Cure Paralysis, University of Miami Miller School of Medicine, Miami, FL, USA; Center for Computational Science, University of Miami, Miami, FL, USA; Department of Neurological Surgery, University of Miami Miller School of Medicine, Miami, FL, USA. Electronic address:

Axon regeneration is a necessary step toward functional recovery after spinal cord injury. The AP-1 transcription factor c-Jun has long been known to play an important role in directing the transcriptional response of Dorsal Root Ganglion (DRG) neurons to peripheral axotomy that results in successful axon regeneration. Here we performed ChIPseq for Jun in mouse DRG neurons after a sciatic nerve crush or sham surgery in order to measure the changes in Jun's DNA binding in response to peripheral axotomy. Read More

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http://dx.doi.org/10.1016/j.mcn.2018.08.001DOI Listing
October 2018
3 Reads

The ferroxidase ceruloplasmin influences Reelin processing, cofilin phosphorylation and neuronal organization in the developing brain.

Mol Cell Neurosci 2018 10 2;92:104-113. Epub 2018 Aug 2.

Département de Chimie and Centre BioMed, Université du Québec à Montréal, C.P. 8888, Succ. Centre-ville, Montreal, Quebec H3C 3P8, Canada. Electronic address:

Ceruloplasmin (Cp) is an important extracellular regulator of iron metabolism. We showed previously that it stimulates Reelin proteolytic processing and cell aggregation in cultures of developing neurons. Reelin is a secreted protein required for the correct positioning of neurons in the brain. Read More

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http://dx.doi.org/10.1016/j.mcn.2018.07.005DOI Listing
October 2018
2 Reads

Changes in synaptic AMPA receptor concentration and composition in chronic temporal lobe epilepsy.

Mol Cell Neurosci 2018 10 29;92:93-103. Epub 2018 Jul 29.

Laboratory for Synaptic Plasticity, Division of Anatomy, Department of Molecular Medicine, Institute of Basic Medical Sciences, Faculty of Medicine, University of Oslo, Oslo, Norway. Electronic address:

Excitotoxicity caused by excessive stimulation of glutamate receptors, resulting in pathologically increased Ca-concentrations, is a decisive factor in neurodegenerative diseases. We investigated long-term changes in synaptic contents of AMPA receptor subunits that play important roles in calcium regulation in chronic epilepsy. Such plastic changes may be either adaptive or detrimental. Read More

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http://dx.doi.org/10.1016/j.mcn.2018.07.004DOI Listing
October 2018
1 Read

Physiological signature of a novel potentiator of AMPA receptor signalling.

Mol Cell Neurosci 2018 10 22;92:82-92. Epub 2018 Jul 22.

Department of Pharmacology, School of Pharmacy, University College London, London, UK. Electronic address:

We have synthesized a novel small molecule based on the pyrrolidinone-containing core structure of clausenamide, which is a candidate anti-dementia drug. The synthetic route yielded multi-gram quantities of an isomeric racemate mixture in a short number of steps. When tested in hippocampal slices from young adult rats the compound enhanced AMPA receptor-mediated signalling at mossy fibre synapses, and potentiated inward currents evoked by local application of l-glutamate onto CA3 pyramidal neurons. Read More

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http://dx.doi.org/10.1016/j.mcn.2018.07.003DOI Listing
October 2018

EphBs and ephrin-Bs: Trans-synaptic organizers of synapse development and function.

Mol Cell Neurosci 2018 09 19;91:108-121. Epub 2018 Jul 19.

The Jefferson Synaptic Biology Center, Department of Neuroscience, The Vickie and Jack Farber Institute for Neuroscience, Sidney Kimmel Medical College at Thomas Jefferson University, Jefferson Hospital for Neuroscience, Suite 463, 900 Walnut St., Philadelphia, PA 19107, United States. Electronic address:

Synapses are specialized cell-cell junctions that underlie the function of neural circuits by mediating communication between neurons. Both the formation and function of synapses require tight coordination of signaling between pre- and post-synaptic neurons. Trans-synaptic organizing molecules are important mediators of such signaling. Read More

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http://dx.doi.org/10.1016/j.mcn.2018.07.002DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6159941PMC
September 2018
1 Read

Regulation of actin dynamics during structural plasticity of dendritic spines: Signaling messengers and actin-binding proteins.

Mol Cell Neurosci 2018 09 9;91:122-130. Epub 2018 Jul 9.

Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, ON M5G 1X5, Canada; Department of Molecular Genetics, Faculty of Medicine, University of Toronto, Toronto, ON M5G 1X5, Canada. Electronic address:

Activity-dependent plasticity of synaptic structure and function plays an essential role in neuronal development and in cognitive functions including learning and memory. The formation, maintenance and modulation of dendritic spines are mainly controlled by the dynamics of actin filaments (F-actin) through interaction with various actin-binding proteins (ABPs) and postsynaptic signaling messengers. Induction of long-term potentiation (LTP) triggers a cascade of events involving Ca signaling, intracellular pathways such as cAMP and cGMP, and regulation of ABPs such as CaMKII, Cofilin, Aip1, Arp2/3, α-actinin, Profilin and Drebrin. Read More

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http://dx.doi.org/10.1016/j.mcn.2018.07.001DOI Listing
September 2018
22 Reads

Class 4 Semaphorins and Plexin-B receptors regulate GABAergic and glutamatergic synapse development in the mammalian hippocampus.

Mol Cell Neurosci 2018 10 4;92:50-66. Epub 2018 Jul 4.

Department of Biology, Brandeis University, Waltham, MA 02454, United States; Volen Center for Complex Systems, Brandeis University, Waltham, MA 02454, United States; National Center for Behavioral Genomics, Brandeis University, Waltham, MA 02454, United States. Electronic address:

To understand how proper circuit formation and function is established in the mammalian brain, it is necessary to define the genes and signaling pathways that instruct excitatory and inhibitory synapse development. We previously demonstrated that the ligand-receptor pair, Sema4D and Plexin-B1, regulates inhibitory synapse development on an unprecedentedly fast time-scale while having no effect on excitatory synapse development. Here, we report previously undescribed synaptogenic roles for Sema4A and Plexin-B2 and provide new insight into Sema4D and Plexin-B1 regulation of synapse development in rodent hippocampus. Read More

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http://dx.doi.org/10.1016/j.mcn.2018.06.008DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6191356PMC
October 2018
6 Reads

Involvement of l-afadin, but not s-afadin, in the formation of puncta adherentia junctions of hippocampal synapses.

Mol Cell Neurosci 2018 10 30;92:40-49. Epub 2018 Jun 30.

Division of Pathogenetic Signaling, Department of Biochemistry and Molecular Biology, Kobe University Graduate School of Medicine, 1-5-6 Minatojima-minamimachi, Chuo-ku, Kobe, Hyogo 650-0047, Japan. Electronic address:

A hippocampal mossy fiber synapse has a complex structure in which presynaptic boutons attach to the dendritic trunk by puncta adherentia junctions (PAJs) and wrap multiply-branched spines, forming synaptic junctions. It was previously shown that afadin regulates the formation of the PAJs cooperatively with nectin-1, nectin-3, and N-cadherin. Afadin is a nectin-binding protein with two splice variants, l-afadin and s-afadin: l-afadin has an actin filament-binding domain, whereas s-afadin lacks it. Read More

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http://dx.doi.org/10.1016/j.mcn.2018.06.006DOI Listing
October 2018
16 Reads

Depletion of astrocytic transglutaminase 2 improves injury outcomes.

Mol Cell Neurosci 2018 10 30;92:128-136. Epub 2018 Jun 30.

Department of Pharmacology and Physiology, University of Rochester, Rochester, NY 14642, USA; Department of Biomedical Genetics, University of Rochester, Rochester, NY 14642, USA; Department of Anesthesiology and Perioperative Medicine, University of Rochester, Rochester, NY 14642, USA. Electronic address:

Astrocytes play an indispensable role in maintaining a healthy, functional neural network in the central nervous system (CNS). A primary function of CNS astrocytes is to support the survival and function of neurons. In response to injury, astrocytes take on a reactive phenotype, which alters their molecular functions. Read More

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http://dx.doi.org/10.1016/j.mcn.2018.06.007DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6218936PMC
October 2018
18 Reads

Sex-dependent co-occurrence of hypoxia and β-amyloid plaques in hippocampus and entorhinal cortex is reversed by long-term treatment with ubiquinol and ascorbic acid in the 3 × Tg-AD mouse model of Alzheimer's disease.

Mol Cell Neurosci 2018 10 25;92:67-81. Epub 2018 Jun 25.

Department of Medical Sciences, Faculty of Medicine, University of Castilla-La Mancha, Spain; Oxidative Stress and Neurodegeneration Group, Regional Centre for Biomedical Research, University of Castilla-La Mancha, Spain. Electronic address:

Structural and functional abnormalities in the cerebral microvasculature have been observed in Alzheimer's disease (AD) patients and animal models. One cause of hypoperfusion is the thickening of the cerebrovascular basement membrane (CVBM) due to increased collagen-IV deposition around capillaries. This study investigated whether these and other alterations in the cerebrovascular system associated with AD can be prevented by long-term dietary supplementation with the antioxidant ubiquinol (Ub) stabilized with Kaneka QH P30 powder containing ascorbic acid (ASC) in a mouse model of advanced AD (3 × Tg-AD mice, 12 months old). Read More

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http://dx.doi.org/10.1016/j.mcn.2018.06.005DOI Listing
October 2018
11 Reads

Semaphorin 3A as an inhibitive factor for migration of olfactory ensheathing cells through cofilin activation is involved in formation of olfactory nerve layer.

Mol Cell Neurosci 2018 10 27;92:27-39. Epub 2018 Jun 27.

Institute of Neuroscience and Institute of Hypoxia Medicine, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China; School of Mental Health, Wenzhou Medical University, Zhejiang 325035, China. Electronic address:

Olfactory ensheathing cells (OECs) migrate from olfactory epithelium towards olfactory bulb (OB), contributing to formation of the presumptive olfactory nerve layer during development. However, it remains unclear that molecular mechanism of regulation of OEC migration in OB. In the present study, we found that OECs highly expressed the receptors of semaphorin 3A (Sema3A) in vitro and in vivo, whereas Sema3A displayed a gradient expression pattern with higher in inner layer of OB and lower in outer layer of OB. Read More

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http://dx.doi.org/10.1016/j.mcn.2018.06.004DOI Listing
October 2018
11 Reads