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Parkinson Disease: HELP
Articles from National Institute on Alcohol Abuse and Alcoholism
Based on 4 articles published since 2010
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These are the 4 published articles about Parkinson Disease that originated from National Institute on Alcohol Abuse and Alcoholism during 2010-2020.
 
+ Citations + Abstracts
1 Review Serotonergic action on dorsal striatal function. 2012

Mathur, Brian N / Lovinger, David M. ·Laboratory for Integrative Neuroscience, National Institute on Alcohol Abuse and Alcoholism, US National Institutes of Health, Rockville, MD 20852-9411, USA. ·Parkinsonism Relat Disord · Pubmed #22166410.

ABSTRACT: Serotonin (5-HT) is a monoamine neurotransmitter released throughout the brain. The serotonergic system is implicated in a host of neuropsychiatric disorders including, but not limited to, Parkinson's disease and L-DOPA-induced dyskinesia. These are pathological and drug-induced states that center on dysfunction of the striatum, a basal ganglia structure necessary for voluntary movement control and action learning. 5-HT is released by dorsal raphe nucleus neurons into the dorsal striatum where it acts upon diverse 5-HT receptors that are expressed on various pre- and postsynaptic components. Here, we review the literature on serotonergic effects on dorsal striatal function and discuss possible roles for the striatal serotonergic system in physiological and parkinsonian states.

2 Article Selective expression of Parkinson's disease-related Leucine-rich repeat kinase 2 G2019S missense mutation in midbrain dopaminergic neurons impairs dopamine release and dopaminergic gene expression. 2015

Liu, Guoxiang / Sgobio, Carmelo / Gu, Xinglong / Sun, Lixin / Lin, Xian / Yu, Jia / Parisiadou, Loukia / Xie, Chengsong / Sastry, Namratha / Ding, Jinhui / Lohr, Kelly M / Miller, Gary W / Mateo, Yolanda / Lovinger, David M / Cai, Huaibin. ·Transgenics Section and Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA. · Transgenics Section and. · Bioinformatics Core, Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA. · Center for Neurodegenerative Disease, Emory University, Atlanta, GA 30322, USA and. · Laboratory of Integrative Neuroscience, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Rockville, MD 20852, USA. · Transgenics Section and caih@mail.nih.gov. ·Hum Mol Genet · Pubmed #26123485.

ABSTRACT: Preferential dysfunction/degeneration of midbrain substantia nigra pars compacta (SNpc) dopaminergic (DA) neurons contributes to the main movement symptoms manifested in Parkinson's disease (PD). Although the Leucine-rich repeat kinase 2 (LRRK2) G2019S missense mutation (LRRK2 G2019S) is the most common causative genetic factor linked to PD, the effects of LRRK2 G2019S on the function and survival of SNpc DA neurons are poorly understood. Using a binary gene expression system, we generated transgenic mice expressing either wild-type human LRRK2 (WT mice) or the LRRK2 G2019S mutation (G2019S mice) selectively in the midbrain DA neurons. Here we show that overexpression of LRRK2 G2019S did not induce overt motor abnormalities or substantial SNpc DA neuron loss. However, the LRRK2 G2019S mutation impaired dopamine homeostasis and release in aged mice. This reduction in dopamine content/release coincided with the degeneration of DA axon terminals and decreased expression of DA neuron-enriched genes tyrosine hydroxylase (TH), vesicular monoamine transporter 2, dopamine transporter and aldehyde dehydrogenase 1. These factors are responsible for dopamine synthesis, transport and degradation, and their expression is regulated by transcription factor paired-like homeodomain 3 (PITX3). Levels of Pitx3 mRNA and protein were similarly decreased in the SNpc DA neurons of aged G2019S mice. Together, these findings suggest that PITX3-dependent transcription regulation could be one of the many potential mechanisms by which LRRK2 G2019S acts in SNpc DA neurons, resulting in downregulation of its downstream target genes critical for dopamine homeostasis and release.

3 Article Neuroprotective effects of berry fruits on neurodegenerative diseases. 2014

Subash, Selvaraju / Essa, Musthafa Mohamed / Al-Adawi, Samir / Memon, Mushtaq A / Manivasagam, Thamilarasan / Akbar, Mohammed. ·Department of Food Science and Nutrition, College of Agricultural and Marine Sciences, Sultan Qaboos University, Muscat, Sultanate of Oman ; Ageing and Dementia Research Group, Sultan Qaboos University, Muscat, Sultanate of Oman. · Ageing and Dementia Research Group, Sultan Qaboos University, Muscat, Sultanate of Oman ; College of Medicine and Health Sciences, Sultan Qaboos University, Muscat, Sultanate of Oman. · College of Veterinary Medicine, Washington State University, Pullman, WA, USA. · Department of Biochemistry and Biotechnology, Annamalai University, Tamilnadu, India. · Section of Molecular Pharmacology and Toxicology, Laboratory of Membrane Biochemistry and Biophysics, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Rockville, MD, USA. ·Neural Regen Res · Pubmed #25317174.

ABSTRACT: Recent clinical research has demonstrated that berry fruits can prevent age-related neurodegenerative diseases and improve motor and cognitive functions. The berry fruits are also capable of modulating signaling pathways involved in inflammation, cell survival, neurotransmission and enhancing neuroplasticity. The neuroprotective effects of berry fruits on neurodegenerative diseases are related to phytochemicals such as anthocyanin, caffeic acid, catechin, quercetin, kaempferol and tannin. In this review, we made an attempt to clearly describe the beneficial effects of various types of berries as promising neuroprotective agents.

4 Article Endocannabinoid-dopamine interactions in striatal synaptic plasticity. 2012

Mathur, Brian N / Lovinger, David M. ·Section on Synaptic Pharmacology, Laboratory for Integrative Neuroscience, National Institute on Alcohol Abuse and Alcoholism, U.S. National Institutes of Health Rockville, MD, USA. ·Front Pharmacol · Pubmed #22529814.

ABSTRACT: The nigrostriatal dopaminergic system is implicated in action control and learning. A large body of work has focused on the contribution of this system to modulation of the corticostriatal synapse, the predominant synapse type in the striatum. Signaling through the D2 dopamine receptor is necessary for endocannabinoid-mediated depression of corticostriatal glutamate release. Here we review the known details of this mechanism and discuss newly discovered signaling pathways interacting with this system that ultimately exert dynamic control of cortical input to the striatum and striatal output. This topic is timely with respect to Parkinson's disease given recent data indicating changes in the striatal endocannabinoid system in patients with this disorder.