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Drug induced neurodegeneration

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https://www.readbyqxmd.com/read/28217866/zebrafish-models-in-neuropsychopharmacology-and-cns-drug-discovery
#1
REVIEW
Kanza M Khan, Adam D Collier, Darya A Meshalkina, Elana V Kysil, Sergey L Khatsko, Tatyana Kolesnikova, Yury Yu Morzherin, Jason E Warnick, Allan V Kalueff, David J Echevarria
Despite high prevalence of neuropsychiatric disorders, their etiology and molecular mechanisms remain poorly understood. The zebrafish (Danio rerio) is increasingly utilized as a powerful animal model in neuropharmacology research and in-vivo drug screening. Collectively, this makes zebrafish a useful tool for drug discovery and the identification of disordered molecular pathways. Here, we discuss zebrafish models of selected human neuropsychiatric disorders and drug-induced phenotypes. Covering a broad range of brain disorders (from anxiety and psychoses to neurodegeneration), we also summarize recent developments in zebrafish genetics and small molecule screening, which markedly enhance the disease modeling and the discovery of novel drug targets...
February 20, 2017: British Journal of Pharmacology
https://www.readbyqxmd.com/read/28205624/the-small-molecule-auten-99-autophagy-enhancer-99-prevents-the-progression-of-neurodegenerative-symptoms
#2
Tibor Kovács, Viktor Billes, Marcell Komlós, Bernadette Hotzi, Anna Manzéger, Anna Tarnóci, Diána Papp, Fanni Szikszai, Janka Szinyákovics, Ákos Rácz, Béla Noszál, Szilvia Veszelka, Fruzsina R Walter, Mária A Deli, Laszlo Hackler, Robert Alfoldi, Orsolya Huzian, Laszlo G Puskas, Hanna Liliom, Krisztián Tárnok, Katalin Schlett, Adrienn Borsy, Ervin Welker, Attila L Kovács, Zsolt Pádár, Attila Erdős, Adam Legradi, Annamaria Bjelik, Károly Gulya, Balázs Gulyás, Tibor Vellai
Autophagy functions as a main route for the degradation of superfluous and damaged constituents of the cytoplasm. Defects in autophagy are implicated in the development of various age-dependent degenerative disorders such as cancer, neurodegeneration and tissue atrophy, and in accelerated aging. To promote basal levels of the process in pathological settings, we previously screened a small molecule library for novel autophagy-enhancing factors that inhibit the myotubularin-related phosphatase MTMR14/Jumpy, a negative regulator of autophagic membrane formation...
February 16, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28197073/association-of-trka-and-app-is-promoted-by-ngf-and-reduced-by-cell-death-promoting-agents
#3
Nadia Canu, Ilaria Pagano, Luca Rosario La Rosa, Marsha Pellegrino, Maria Teresa Ciotti, Delio Mercanti, Fabiola Moretti, Valentina Sposato, Viviana Triaca, Carla Petrella, Ichiro N Maruyama, Andrea Levi, Pietro Calissano
The amyloid precursor protein (APP) interacts with the tropomyosin receptor kinase A (TrkA) in normal rat, mouse, and human brain tissue but not in Alzheimer's disease (AD) brain tissue. However, it has not been reported whether the two proteins interact directly, and if so, which domains are involved. Clarifying these points will increase our understanding of the role and regulation of the TrkA/APP interaction in normal brain functioning as well as in AD. Here we addressed these questions using bimolecular fluorescence complementation (BiFC) and the proximity ligation assay (PLA)...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28181916/4-phenylbutyric-acid-and-metformin-decrease-sensitivity-to-pentylenetetrazol-induced-seizures-in-a-malin-knockout-model-of-lafora-disease
#4
Gentzane Sánchez-Elexpuru, José M Serratosa, Pascual Sanz, Marina P Sánchez
Lafora disease (LD) is a rare adolescent-onset progressive myoclonic epilepsy caused by loss-of-function mutations either in the EPM2A gene encoding laforin or in the EPM2B gene encoding malin. Mouse models with deletion in the Epm2a or the Epm2b gene show intracellular aggregates of polyglucosans (Lafora bodies) and neurological complications that resemble those observed in patients with LD. In the absence of laforin or malin expression, mice also show different degrees of hyperexcitability, as reflected by an enhanced response to the convulsant drug pentylenetetrazol (PTZ)...
February 8, 2017: Neuroreport
https://www.readbyqxmd.com/read/28173812/anthocyanins-encapsulated-by-plga-peg-nanoparticles-potentially-improved-its-free-radical-scavenging-capabilities-via-p38-jnk-pathway-against-a%C3%AE-1-42-induced-oxidative-stress
#5
Faiz Ul Amin, Shahid Ali Shah, Haroon Badshah, Mehtab Khan, Myeong Ok Kim
BACKGROUND: In order to increase the bioavailability of hydrophilic unstable drugs like anthocyanins, we employed a polymer-based nanoparticles approach due to its unique properties such as high stability, improved bioavailability and high water-soluble drug loading efficiency. Anthocyanins constitute a subfamily of flavonoids that possess anti-oxidative, anti-inflammatory and neuroprotective properties. However, anthocyanins are unstable because their phenolic hydroxyl groups are easily oxidized into quinones, causing a reduced biological activity...
February 7, 2017: Journal of Nanobiotechnology
https://www.readbyqxmd.com/read/28159472/metformin-activation-of-ampk-suppresses-age-induced-inflammatory-response-in-hnscs
#6
Ming-Min Chung, Christopher J Nicol, Yi-Chuan Cheng, Kuan-Hung Lin, Yen-Lin Chen, Dee Pei, Chien-Hung Lin, Yi-Nuo Shih, Chia-Hui Yen, Shiang-Jiuun Chen, Rong-Nan Huang, Ming-Chang Chiang
A growing body of evidence suggests type 2 diabetes mellitus (T2DM) is linked to neurodegenerative diseases such as Alzheimer's disease (AD). Although the precise mechanisms remain unclear, T2DM may exacerbate neurodegenerative processes. AMP-activated protein kinase (AMPK) signaling is an evolutionary preserved pathway that is important during homeostatic energy biogenesis responses at both the cellular and whole-body levels. Metformin, a ubiquitously prescribed anti-diabetic drug, exerts its effects by AMPK activation...
January 31, 2017: Experimental Cell Research
https://www.readbyqxmd.com/read/28105557/the-anticancer-drug-sunitinib-promotes-autophagyand-protects-from-neurotoxicity-in-an-hiv-1-tat-model-of-neurodegeneration
#7
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
#8
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
#9
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
#10
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
#11
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
#12
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
#13
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
#14
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
#15
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
#16
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
#17
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 23, 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
#18
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
#19
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
#20
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
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