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Parkinson Disease: HELP
Articles from Miscellaneous institutions in Long Island towns
Based on 7 articles published since 2010
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These are the 7 published articles about Parkinson Disease that originated from Miscellaneous institutions in Long Island towns during 2010-2020.
 
+ Citations + Abstracts
1 Article Genetic targeting of astrocytes to combat neurodegenerative disease. 2020

Kery, Rachel / Chen, Allen P F / Kirschen, Gregory W. ·Medical Scientist Training Program (MSTP), Stony Brook Medicine; Department of Neurobiology & Behavior, Stony Brook University, Stony Brook, NY, USA. · Medical Scientist Training Program (MSTP), Stony Brook Medicine, Stony Brook, NY, USA. ·Neural Regen Res · Pubmed #31552885.

ABSTRACT: Astrocytes, glial cells that interact extensively with neurons and other support cells throughout the central nervous system, have recently come under the spotlight for their potential contribution to, or potential regenerative role in a host of neurodegenerative disorders. It is becoming increasingly clear that astrocytes, in concert with microglial cells, activate intrinsic immunological pathways in the setting of neurodegenerative injury, although the direct and indirect consequences of such activation are still largely unknown. We review the current literature on the astrocyte's role in several neurodegenerative diseases, as well as highlighting recent advances in genetic manipulation of astrocytes that may prove critical to modulating their response to neurological injury, potentially combatting neurodegenerative damage.

2 Article Metabolic network abnormalities in drug-naïve Parkinson's Disease. 2019

Schindlbeck, Katharina A / Lucas-Jiménez, Olaia / Tang, Chris C / Morbelli, Silvia / Arnaldi, Dario / Pardini, Matteo / Pagani, Marco / Ibarretxe-Bilbao, Naroa / Ojeda, Natalia / Nobili, Flavio / Eidelberg, David. ·Center for Neurosciences, The Feinstein Institutes for Medical Research, Manhasset, New York, USA. · Department of Methods and Experimental Psychology, Faculty of Psychology and Education, University of Deusto, Bilbao, Spain. · IRCCS Ospedale Policlinico San Martino, Genoa, Italy. · Department of Health Science (DISSAL), University of Genoa, Genoa, Italy. · Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, and Mother-Child Health (DINOGMI), University of Genoa, Genoa, Italy. · Institute of Cognitive Sciences and Technologies, Consiglio Nazionale delle Ricerche (CNR), Rome, Italy. · Department of Nuclear Medicine, Karolinska Hospital, Stockholm, Sweden. ·Mov Disord · Pubmed #31872507.

ABSTRACT: BACKGROUND: An ideal imaging biomarker for a neurodegenerative disorder should be able to measure abnormalities in the earliest stages of the disease. OBJECTIVE: We investigated metabolic network changes in two independent cohorts of drug-naïve Parkinson's disease (PD) patients who have not been exposed to dopaminergic medication. METHODS: We scanned 85 de novo, drug-naïve PD patients and 85 age-matched healthy control subjects from Italy (n = 96) and the United States (n = 74) with [ RESULTS: De novo PD-related metabolic patterns were identified in each of the two independent cohorts of drug-naïve PD patients, and each differentiated PD patients from healthy control subjects. Expression values for these disease patterns were elevated in drug-naïve PD patients relative to healthy controls in the identification as well as in each of the validation subgroups. The two de novo PD-related metabolic patterns were topographically very similar to each other and to the original PD-related pattern. CONCLUSIONS: Reproducible PD-related patterns are expressed in de novo, drug-naïve PD patients. In PD, disease-related metabolic patterns have stereotyped topographies that develop independently of chronic levodopa treatment. © 2019 International Parkinson and Movement Disorder Society.

3 Article LRRK2 and GBA Variants Exert Distinct Influences on Parkinson's Disease-Specific Metabolic Networks. 2019

Schindlbeck, Katharina A / Vo, An / Nguyen, Nha / Tang, Chris C / Niethammer, Martin / Dhawan, Vijay / Brandt, Vicky / Saunders-Pullman, Rachel / Bressman, Susan B / Eidelberg, David. ·Center for Neurosciences, The Feinstein Institutes for Medical Research, Manhasset, NY 10030, USA. · Department of Genetics, Albert Einstein College of Medicine, Bronx, NY 10461, USA. · Department of Neurology, Mount Sinai Beth Israel, Mount Sinai Hospital, New York, NY 10003, USA. ·Cereb Cortex · Pubmed #31813991.

ABSTRACT: The natural history of idiopathic Parkinson's disease (PD) varies considerably across patients. While PD is generally sporadic, there are known genetic influences: the two most common, mutations in the LRRK2 or GBA1 gene, are associated with slower and more aggressive progression, respectively. Here, we applied graph theory to metabolic brain imaging to understand the effects of genotype on the organization of previously established PD-specific networks. We found that closely matched PD patient groups with the LRRK2-G2019S mutation (PD-LRRK2) or GBA1 variants (PD-GBA) expressed the same disease networks as sporadic disease (sPD), but PD-LRRK2 and PD-GBA patients exhibited abnormal increases in network connectivity that were not present in sPD. Using a community detection strategy, we found that the location and modular distribution of these connections differed strikingly across genotypes. In PD-LRRK2, connections were gained within the network core, with the formation of distinct functional pathways linking the cerebellum and putamen. In PD-GBA, by contrast, the majority of functional connections were formed outside the core, involving corticocortical pathways at the network periphery. Strategically localized connections within the core in PD-LRRK2 may maintain PD network activity at lower levels than in PD-GBA, resulting in a less aggressive clinical course.

4 Article Noninvasive PK11195-PET Image Analysis Techniques Can Detect Abnormal Cerebral Microglial Activation in Parkinson's Disease. 2018

Kang, Yeona / Mozley, P David / Verma, Ajay / Schlyer, David / Henchcliffe, Claire / Gauthier, Susan A / Chiao, Ping C / He, Bin / Nikolopoulou, Anastasia / Logan, Jean / Sullivan, Jenna M / Pryor, Kane O / Hesterman, Jacob / Kothari, Paresh J / Vallabhajosula, Shankar. ·Weill Cornell Medicine, New York, NY. · Biogen, Inc., Cambridge, MA. · Brookhaven National Laboratories, NY. · New York University, New York, NY. · inviCRO LLC, Boston, MA. ·J Neuroimaging · Pubmed #29727504.

ABSTRACT: BACKGROUND AND PURPOSE: Neuroinflammation has been implicated in the pathophysiology of Parkinson's disease (PD), which might be influenced by successful neuroprotective drugs. The uptake of [ METHODS: The sample consisted of 20 participants with PD and 19 HVs. Two independent teams analyzed the data to compare the volume of distribution calculated using image-derived input functions (IDIFs), and binding potentials calculated using the Logan reference region model. RESULTS: With all methods, the higher signal-to-background in patients resulted in lower variability and better repeatability than in controls. We were able to use noninvasive techniques showing significantly increased uptake of PK in multiple brain regions of participants with PD compared to HVs. CONCLUSION: Although not necessarily reflecting absolute values, these noninvasive image analysis methods can discriminate between PD patients and HVs. We see a difference of 24% in the substantia nigra between PD and HV with a repeatability coefficient of 13%, showing that it will be possible to estimate responses in longitudinal, within subject trials of novel neuroprotective drugs.

5 Article A Common Function of Basal Ganglia-Cortical Circuits Subserving Speed in Both Motor and Cognitive Domains. 2017

Hanakawa, Takashi / Goldfine, Andrew M / Hallett, Mark. ·Department of Advanced Neuroimaging, Integrative Brain Imaging Center, National Center of Neurology and Psychiatry, Kodaira, Tokyo 187-8551, Japan. · Human Motor Control Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. · Department of Neurology, Stony Brook School of Medicine, Stony Brook, NY 11794. ·eNeuro · Pubmed #29379873.

ABSTRACT: Distinct regions of the frontal cortex connect with their basal ganglia and thalamic counterparts, constituting largely segregated basal ganglia-thalamo-cortical (BTC) circuits. However, any common role of the BTC circuits in different behavioral domains remains unclear. Indeed, whether dysfunctional motor and cognitive BTC circuits are responsible for motor slowing and cognitive slowing, respectively, in Parkinson's disease (PD) is a matter of debate. Here, we used an effortful behavioral paradigm in which the effects of task rate on accuracy were tested in movement, imagery, and calculation tasks in humans. Using nonlinear fitting, we separated baseline accuracy (

6 Article LRRK2 knockdown in zebrafish causes developmental defects, neuronal loss, and synuclein aggregation. 2016

Prabhudesai, Shubhangi / Bensabeur, Fatima Zahra / Abdullah, Rashed / Basak, Indranil / Baez, Solange / Alves, Guido / Holtzman, Nathalia G / Larsen, Jan Petter / Møller, Simon Geir. ·Department of Biological Sciences, St. John's University, Queens, New York. · The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway. · Department of Biology, Queens College and The Graduate Center, CUNY, Queens, New York. ·J Neurosci Res · Pubmed #27265751.

ABSTRACT: Although mutations in the leucine-rich repeat kinase 2 (LRRK2) gene are the most common cause of genetic Parkinson's disease, their function is largely unknown. LRRK2 is pleiotropic in nature, shown to be involved in neurodegeneration and in more peripheral processes, including kidney functions, in rats and mice. Recent studies in zebrafish have shown conflicting evidence that removal of the LRRK2 WD40 domain may or may not affect dopaminergic neurons and/or locomotion. This study shows that ∼50% LRRK2 knockdown in zebrafish causes not only neuronal loss but also developmental perturbations such as axis curvature defects, ocular abnormalities, and edema in the eyes, lens, and otic vesicles. We further show that LRRK2 knockdown results in significant neuronal loss, including a reduction of dopaminergic neurons. Immunofluorescence demonstrates that endogenous LRRK2 is expressed in the lens, brain, heart, spinal cord, and kidney (pronephros), which mirror the LRRK2 morphant phenotypes observed. LRRK2 knockdown results further in the concomitant upregulation of β-synuclein, PARK13, and SOD1 and causes β-synuclein aggregation in the diencephalon, midbrain, hindbrain, and postoptic commissure. LRRK2 knockdown causes mislocalization of the Na(+) /K(+) ATPase protein in the pronephric ducts, suggesting that the edema might be linked to renal malfunction and that LRRK2 might be associated with pronephric duct epithelial cell differentiation. Combined, our study shows that LRRK2 has multifaceted roles in zebrafish and that zebrafish represent a complementary model to further our understanding of this central protein. © 2016 Wiley Periodicals, Inc.

7 Article Recovery of dopamine transporters with methamphetamine detoxification is not linked to changes in dopamine release. 2015

Volkow, Nora D / Wang, Gene-Jack / Smith, Lisa / Fowler, Joanna S / Telang, Frank / Logan, Jean / Tomasi, Dardo. ·Laboratory of Neuroimaging, Intramural Program, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD, USA; Office of Director, National Institute on Drug Abuse, Bethesda, MD, USA. Electronic address: nvolkow@nida.nih.gov. · Laboratory of Neuroimaging, Intramural Program, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD, USA. · Department of Psychiatry, University of California, Los Angeles, CA, USA. · Medical Department, Brookhaven National Laboratory, Upton, NY, USA. ·Neuroimage · Pubmed #26208874.

ABSTRACT: Methamphetamine's widepread abuse and concerns that it might increase Parkinson's disease led us to assess if the reported loss of dopamine transporters (DAT) in methamphetamine abusers (MA) reflected damage to dopamine neurons. Using PET with [(11)C]cocaine to measure DAT, and with [(11)C]raclopride to measure dopamine release (assessed as changes in specific binding of [(11)C]raclopride between placebo and methylphenidate), which was used as a marker of dopamine neuronal function, we show that MA (n=16), tested during early detoxification, had lower DAT (20-30%) but overall normal DA release in striatum (except for a small decrease in left putamen), when compared to controls (n=15). In controls, DAT were positively correlated with DA release (higher DAT associated with larger DA increases), consistent with DAT serving as markers of DA terminals. In contrast, MA showed a trend for a negative correlation (p=0.07) (higher DAT associated with lower DA increases), consistent with reduced DA re-uptake following DAT downregulation. MA who remained abstinent nine-months later (n=9) showed significant increases in DAT (20%) but methylphenidate-induced dopamine increases did not change. In contrast, in controls, DAT did not change when retested 9 months later but methylphenidate-induced dopamine increases in ventral striatum were reduced (p=0.05). Baseline D2/D3 receptors in caudate were lower in MA than in controls and did not change with detoxification, nor did they change in the controls upon retest. The loss of DAT in the MA, which was not associated with a concomitant reduction in dopamine release as would have been expected if DAT loss reflected DA terminal degneration; as well as the recovery of DAT after protracted detoxification, which was not associated with increased dopamine release as would have been expected if DAT increases reflected terminal regeneration, indicate that the loss of DAT in these MA does not reflect degeneration of dopamine terminals.