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Drug induced neurodegeneration

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https://www.readbyqxmd.com/read/28105557/the-anticancer-drug-sunitinib-promotes-autophagyand-protects-from-neurotoxicity-in-an-hiv-1-tat-model-of-neurodegeneration
#1
Jerel A Fields, Jeff Metcalf, Cassia Overk, Anthony Adame, Brian Spencer, Wolfgang Wrasidlo, Jazmin Florio, Edward Rockenstein, Johnny J He, Eliezer Masliah
Despite the success of antiretroviral therapies to control systemic HIV-1 infection, the prevalence of HIV-associated neurocognitive disorders (HANDs) has not decreased among aging patients with HIV. Autophagy pathway alterations, triggered by HIV-1 proteins including gp120, Tat, and Nef, might contribute to the neurodegenerative process in aging patients with HAND. Although no treatments are currently available to manage HAND, we have previously shown that sunitinib, an anticancer drug that blocks receptor tyrosine-kinase and cyclin kinase pathways, might be of interest...
January 19, 2017: Journal of Neurovirology
https://www.readbyqxmd.com/read/28102525/environmental-chemicals-and-aging
#2
REVIEW
Brandon L Pearson, Dan Ehninger
PURPOSE OF REVIEW: Innovations in agriculture and medicine as well as industrial and domestic technologies are essential for the growing and aging global population. These advances generally require the use of novel natural or synthetic chemical agents with the potential to affect human health. Here, we attempt to highlight environmental chemicals and select drugs with the potential to exacerbate aging by directly affecting molecular aging cascades focusing particular attention on the brain...
January 19, 2017: Current Environmental Health Reports
https://www.readbyqxmd.com/read/28093935/new-methods-for-monitoring-mitochondrial-biogenesis-and-mitophagy-in%C3%A2-vitro-and-in%C3%A2-vivo
#3
Jessica A Williams, Katrina Zhao, Shengkan Jin, Wen-Xing Ding
Removal of damaged mitochondria through mitophagy is critical for maintaining cellular homeostasis and functions. Increasing evidence implicates mitophagy in red blood cell differentiation, neurodegeneration, macrophage-mediated inflammation, ischemia, adipogenesis, drug-induced tissue injury, and cancer. Considerable progress has been made toward understanding the biochemical mechanisms involved in mitophagy regulation. However, few reliable assays to monitor and quantify mitophagy have been developed, particularly in vivo...
January 1, 2017: Experimental Biology and Medicine
https://www.readbyqxmd.com/read/28088213/glycine-alanine-dipeptide-repeat-protein-contributes-to-toxicity-in-a-zebrafish-model-of-c9orf72-associated-neurodegeneration
#4
Yu Ohki, Andrea Wenninger-Weinzierl, Alexander Hruscha, Kazuhide Asakawa, Koichi Kawakami, Christian Haass, Dieter Edbauer, Bettina Schmid
BACKGROUND: The most frequent genetic cause of frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclerosis (ALS) is the expansion of a GGGGCC hexanucleotide repeat in a non-coding region of the chromosome 9 open reading frame 72 (C9orf72) locus. The pathological hallmarks observed in C9orf72 repeat expansion carriers are the formation of RNA foci and deposition of dipeptide repeat (DPR) proteins derived from repeat associated non-ATG (RAN) translation. Currently, it is unclear whether formation of RNA foci, DPR translation products, or partial loss of C9orf72 predominantly drive neurotoxicity in vivo...
January 14, 2017: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/28086980/inflammation-in-epileptogenesis-after-traumatic-brain-injury
#5
REVIEW
Kyria M Webster, Mujun Sun, Peter Crack, Terence J O'Brien, Sandy R Shultz, Bridgette D Semple
BACKGROUND: Epilepsy is a common and debilitating consequence of traumatic brain injury (TBI). Seizures contribute to progressive neurodegeneration and poor functional and psychosocial outcomes for TBI survivors, and epilepsy after TBI is often resistant to existing anti-epileptic drugs. The development of post-traumatic epilepsy (PTE) occurs in a complex neurobiological environment characterized by ongoing TBI-induced secondary injury processes. Neuroinflammation is an important secondary injury process, though how it contributes to epileptogenesis, and the development of chronic, spontaneous seizure activity, remains poorly understood...
January 13, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28081197/morphine-withdrawal-modifies-prion-protein-expression-in-rat-hippocampus
#6
Vincenzo Mattei, Stefano Martellucci, Francesca Santilli, Valeria Manganelli, Tina Garofalo, Niccolò Candelise, Alessandra Caruso, Maurizio Sorice, Sergio Scaccianoce, Roberta Misasi
The hippocampus is a vulnerable brain structure susceptible to damage during aging and chronic stress. Repeated exposure to opioids may alter the brain so that it functions normally when the drugs are present, thus, a prolonged withdrawal might lead to homeostatic changes headed for the restoration of the physiological state. Abuse of morphine may lead to Reacting Oxygen Species-induced neurodegeneration and apoptosis. It has been proposed that during morphine withdrawal, stress responses might be responsible, at least in part, for long-term changes of hippocampal plasticity...
2017: PloS One
https://www.readbyqxmd.com/read/28078543/topiramate-confers-neuroprotection-against-methylphenidate-induced-neurodegeneration-in-dentate-gyrus-and-ca1-regions-of-hippocampus-via-creb-bdnf-pathway-in-rats
#7
Majid Motaghinejad, Manijeh Motevalian, Mohammad Abdollahi, Mansour Heidari, Zahra Madjd
Methylphenidate (MPH) abuse can cause serious neurological damages. The neuroprotective effects of topiramate (TPM) have been reported already, but its mechanism of action still remains unclear. The current study evaluates in vivo role of CREB/BDNF in TPM protection of the rat hippocampal cells from methylphenidate-induced apoptosis, oxidative stress, and inflammation. A total of 60 adult male rats were divided into six groups. Groups 1 and 2 received normal saline (0.7 ml/rat) and MPH (10 mg/kg) respectively for 14 days...
January 11, 2017: Neurotoxicity Research
https://www.readbyqxmd.com/read/28070110/melatonin-suppresses-methamphetamine-triggered-endoplasmic-reticulum-stress-in-c6-cells-glioma-cell-lines
#8
Wanida Tungkum, Pichaya Jumnongprakhon, Chainarong Tocharus, Piyarat Govitrapong, Jiraporn Tocharus
Methamphetamine (METH) is a neurotoxic drug that causes brain damage by inducing neuronal and glial cell death together with glial cell hyperactivity-mediated progressive neurodegeneration. Previous studies have shown that METH induced glial cell hyperactivity and death via oxidative stress, the inflammatory response, and endoplasmic reticulum stress (ER stress) mechanisms, and melatonin could reverse these effects. However, the exact mechanism of the protective role of melatonin in METH-mediated ER stress has not been understood...
2017: Journal of Toxicological Sciences
https://www.readbyqxmd.com/read/28068280/landolphia-owariensis-attenuates-alcohol-induced-cerebellar-neurodegeneration-significance-of-neurofilament-protein-alteration-in-the-purkinje-cells
#9
Charles A Oyinbo, Patrick S Igbigbi, Godwin O Avwioro
BACKGROUND: Alcohol-induced cerebellar neurodegeneration is a neuroadaptation that is associated with chronic alcohol abuse. Conventional drugs have been largely unsatisfactory in preventing neurodegeneration. Yet, multimodal neuro-protective therapeutic agents have been hypothesised to have high therapeutic potential for the treatment of CNS conditions; there is yet a dilemma of how this would be achieved. Contrarily, medicinal botanicals are naturally multimodal in their mechanism of action...
December 1, 2016: Folia Medica
https://www.readbyqxmd.com/read/28067625/pituitary-adenylate-cyclase-activating-polypeptide-pacap-has-neuroprotective-function-in-dopamine-based-neurodegeneration-developed-in-two-parkinsonian-models
#10
G Maasz, Z Zrinyi, D Reglodi, D Petrovics, A Rivnyak, T Kiss, A Jungling, A Tamas, Z Pirger
It has been observed that pituitary-adenylate cyclase activating polypeptide (PACAP) rescued DAergic neurons from neurodegeneration and improved motor alterations induced by 6-hydroxy-dopamine (6-OHDA) in rat parkinsonian models. Recently we investigated the molecular background of the neuroprotective effect of PACAP in DA-based neurodegeneration using rotenone-induced snail and 6-OHDA-induced rat models of Parkinson's disease. The behavioural activity, monoamine (DA and serotonin), metabolic enzyme (S-COMT, MB-COMT and MAO-B) and PARK7/DJ-1 protein contents were measured before and after PACAP-treatment in both models...
December 22, 2016: Disease Models & Mechanisms
https://www.readbyqxmd.com/read/28067072/drug-target-identification-at-the-crossroad-of-neuronal-apoptosis-and-survival
#11
Barbara Maino, Simona Paparone, Cinzia Severini, Maria Teresa Ciotti, Velia D'Agata, Pietro Calissano, Sebastiano Cavallaro
Inappropriate activation of apoptosis may contribute to neurodegeneration, a multifaceted process that results in various chronic disorders, including Alzheimer's and Parkinson's diseases. Several in vitro and in vivo studies demonstrated that neuronal apoptosis is a multi-pathway cell-death program that requires RNA synthesis. Thus, transcriptionally activated genes whose products induce cell death can be triggered by different stimuli and antagonized by neurotrophic factors. Systems biology is now unveiling the series of intracellular signaling pathways and key drug targets at the intersection of neuronal apoptosis and survival...
January 8, 2017: Expert Opinion on Drug Discovery
https://www.readbyqxmd.com/read/28049155/intraneuronal-protein-aggregation-as-a-trigger-for-inflammation-and-neurodegeneration-in-the-aging-brain
#12
REVIEW
Antonio Currais, Wolfgang Fischer, Pamela Maher, David Schubert
Age is, by far, the greatest risk factor for Alzheimer's disease (AD), yet few AD drug candidates have been generated that target pathways specifically associated with the aging process itself. Two ubiquitous features of the aging brain are the intracellular accumulation of aggregated proteins and inflammation. As intraneuronal amyloid protein is detected before markers of inflammation, we argue that old, age-associated, aggregated proteins in neurons can induce inflammation, resulting in multiple forms of brain toxicities...
January 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/28043837/targeting-antioxidant-enzyme-expression-as-a-therapeutic-strategy-for-ischemic-stroke
#13
REVIEW
Stephanie M Davis, Keith R Pennypacker
During ischemic stroke, neurons and glia are subjected to damage during the acute and neuroinflammatory phases of injury. Production of reactive oxygen species (ROS) from calcium dysregulation in neural cells and the invasion of activated immune cells are responsible for stroke-induced neurodegeneration. Scientists have failed thus far to identify antioxidant-based drugs that can enhance neural cell survival and improve recovery after stroke. However, several groups have demonstrated success in protecting against stroke by increasing expression of antioxidant enzymes in neural cells...
December 30, 2016: Neurochemistry International
https://www.readbyqxmd.com/read/28042309/the-link-between-vascular-dysfunction-bladder-ischemia-and-aging-bladder-dysfunction
#14
REVIEW
Karl-Erik Andersson, Donna B Boedtkjer, Axel Forman
The vascular supply to the human bladder is derived mainly from the superior and inferior vesical arteries, the latter being directly connected to the internal iliac artery. Aging is associated with an impairment of blood vessel function and changes may occur in the vasculature at the molecular, cellular and functional level. Pelvic arterial insufficiency may play an important role in the development of bladder dysfunctions such as detrusor overactivity (DO) and the overactive bladder syndrome. Chronic ischemia-related bladder dysfunction may progress to bladder underactivity and it would be desirable to treat not only lower urinary tract symptoms (LUTS) induced by chronic ischemia, but also the progression of the morphological bladder changes...
January 2017: Therapeutic Advances in Urology
https://www.readbyqxmd.com/read/28040492/valproic-acid-and-ask1-deficiency-ameliorate-optic-neuritis-and-neurodegeneration-in-an-animal-model-of-multiple-sclerosis
#15
Yuriko Azuchi, Atsuko Kimura, Xiaoli Guo, Goichi Akiyama, Takahiko Noro, Chikako Harada, Atsuko Nishigaki, Kazuhiko Namekata, Takayuki Harada
Optic neuritis, which is an acute inflammatory demyelinating syndrome of the central nervous system, is one of the major complications in multiple sclerosis (MS). Herein, we investigated the therapeutic potential of valproic acid (VPA) on optic neuritis in experimental autoimmune encephalomyelitis (EAE), a mouse model of MS. EAE was induced in C57BL/6 mice by immunization with MOG35-55 and VPA (300mg/kg) was administered via intraperitoneal injection once daily from day 3 postimmunization until the end of the experimental period (day 28)...
December 28, 2016: Neuroscience Letters
https://www.readbyqxmd.com/read/28024798/zonisamide-attenuates-lactacystin-induced-parkinsonism-in-mice-without-affecting-system-xc
#16
Eduard Bentea, Joeri Van Liefferinge, Lise Verbruggen, Katleen Martens, Sho Kobayashi, Lauren Deneyer, Thomas Demuyser, Giulia Albertini, Katrien Maes, Hideyo Sato, Ilse Smolders, Jan Lewerenz, Ann Massie
Zonisamide (ZNS), an anticonvulsant drug exhibiting symptomatic effects in Parkinson's disease (PD), was recently reported to exert neuroprotection in rodent models. One of the proposed neuroprotective mechanisms involves increased protein expression of xCT, the specific subunit of the cystine/glutamate antiporter system xc(-), inducing glutathione (GSH) synthesis. Here, we investigated the outcome of ZNS treatment in a mouse model of PD based on intranigral proteasome inhibition, and whether the observed effects would be mediated by system xc(-)...
December 24, 2016: Experimental Neurology
https://www.readbyqxmd.com/read/28011382/multiple-sclerosis-therapeutic-applications-of-advancing-drug-delivery-systems
#17
REVIEW
Sanam Dolati, Zohreh Babaloo, Farhad Jadidi-Niaragh, Hormoz Ayromlou, Sanam Sadreddini, Mehdi Yousefi
Multiple sclerosis (MS) is an inflammatory autoimmune disease of the central nervous system, which is accompanying with demyelination, neurodegeneration and sensibility to oxidative stress. In MS, auto-reactive lymphocytes cross the blood-brain barrier (BBB) and reside in the perivenous demyelinating lesions which create various distinct inflammatory demyelinated plaques situated predominantly in the white matter. The current MS-related therapeutic approaches can be classified into disease-modifying therapies (DMTs) and symptomatic therapy...
December 20, 2016: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/27993242/hiv-protease-inhibitors-alter-amyloid-precursor-protein-processing-via-%C3%AE-site-amyloid-precursor-protein-cleaving-enzyme-1-translational-up-regulation
#18
Patrick J Gannon, Cagla Akay-Espinoza, Alan C Yee, Lisa A Briand, Michelle A Erickson, Benjamin B Gelman, Yan Gao, Norman J Haughey, M Christine Zink, Janice E Clements, Nicholas S Kim, Gabriel Van De Walle, Brigid K Jensen, Robert Vassar, R Christopher Pierce, Alexander J Gill, Dennis L Kolson, J Alan Diehl, Joseph L Mankowski, Kelly L Jordan-Sciutto
Mounting evidence implicates antiretroviral (ARV) drugs as potential contributors to the persistence and evolution of clinical and pathological presentation of HIV-associated neurocognitive disorders in the post-ARV era. Based on their ability to induce endoplasmic reticulum (ER) stress in various cell types, we hypothesized that ARV-mediated ER stress in the central nervous system resulted in chronic dysregulation of the unfolded protein response and altered amyloid precursor protein (APP) processing. We used in vitro and in vivo models to show that HIV protease inhibitor (PI) class ARVs induced neuronal damage and ER stress, leading to PKR-like ER kinase-dependent phosphorylation of the eukaryotic translation initiation factor 2α and enhanced translation of β-site APP cleaving enzyme-1 (BACE1)...
January 2017: American Journal of Pathology
https://www.readbyqxmd.com/read/27989232/subacute-fluoxetine-reduces-signs-of-hippocampal-damage-induced-by-a-single-convulsant-dose-of-4-aminopyridine-in-rats
#19
Ahmed Anis Shiha, Rubén Fernández de la Rosa, Mercedes Delgado, Miguel Angel Pozo, Luis García-García
The purpose of this study was to investigate the eventual short-term brain impairment induced by a single convulsant dose of the potassium channel blocker 4-aminopyridine (4-AP). To this aim, in vivo 2-deoxy-2-[18F]fluoro-D-glucose ([18F]FDG) positron emission tomography (PET) and several histological assessments were carried out after i.p. administration of 3 mg/kg 4-AP for evaluating eventual brain metabolism impairment and signs of hippocampal damage. On the other hand, it has been reported that antidepressant drugs show anticonvulsant and neuroprotective effects in different animal models of seizures and epilepsy...
July 20, 2016: CNS & Neurological Disorders Drug Targets
https://www.readbyqxmd.com/read/27938410/3d-culture-models-of-alzheimer-s-disease-a-road-map-to-a-cure-in-a-dish
#20
REVIEW
Se Hoon Choi, Young Hye Kim, Luisa Quinti, Rudolph E Tanzi, Doo Yeon Kim
Alzheimer's disease (AD) transgenic mice have been used as a standard AD model for basic mechanistic studies and drug discovery. These mouse models showed symbolic AD pathologies including β-amyloid (Aβ) plaques, gliosis and memory deficits but failed to fully recapitulate AD pathogenic cascades including robust phospho tau (p-tau) accumulation, clear neurofibrillary tangles (NFTs) and neurodegeneration, solely driven by familial AD (FAD) mutation(s). Recent advances in human stem cell and three-dimensional (3D) culture technologies made it possible to generate novel 3D neural cell culture models that recapitulate AD pathologies including robust Aβ deposition and Aβ-driven NFT-like tau pathology...
December 9, 2016: Molecular Neurodegeneration
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