A5052006978- Parkinson's Disease Mechanisms and Treatments
- Receptor Mechanisms and Signaling
- Adenosine and Purinergic Signaling
- Machine Learning in Bioinformatics
- Alzheimer's disease research and treatments
- Mitochondrial Function and Pathology
- Cellular transport and secretion
- Neuroscience and Neuropharmacology Research
- Neuroinflammation and Neurodegeneration Mechanisms
- Autophagy in Disease and Therapy
- Neurological disorders and treatments
- Genetic Neurodegenerative Diseases
- Neurological diseases and metabolism
- Neuropeptides and Animal Physiology
- Nuclear Receptors and Signaling
- Chemical Synthesis and Analysis
- Click Chemistry and Applications
- Axon Guidance and Neuronal Signaling
- Cholinesterase and Neurodegenerative Diseases
- Renin-Angiotensin System Studies
- Lysosomal Storage Disorders Research
- Bipolar Disorder and Treatment
- Neurotransmitter Receptor Influence on Behavior
- Attention Deficit Hyperactivity Disorder
- Nicotinic Acetylcholine Receptors Study
University of Alabama at Birmingham
2016-2024
Indian Institute of Science Bangalore
2023
University of Delhi
2007-2022
Johns Hopkins Medicine
2015
Johns Hopkins University
2015
Centro de Investigación Biomédica en Red
2014
Universitat de Barcelona
2014
National Institute on Drug Abuse
2011-2014
National Institutes of Health
2011-2014
University of East Anglia
2014
Parkinson's disease is a progressive neurodegenerative disorder with multifactorial causes, among which genetic risk factors play part. The RAB GTPases are regulators and substrates of LRRK2, variants in the LRRK2 gene important for disease. We aimed to explore variability within cases familial
The dopamine D<sub>1</sub> receptor–D<sub>3</sub> receptor (D1R-D3R) heteromer is being considered as a potential therapeutic target for neuropsychiatric disorders. Previous studies suggested that this could be involved in the ability of D3R agonists to potentiate locomotor activation induced by D1R agonists. It has also been postulated its overexpression plays role L-dopa–induced dyskinesia and drug addiction. However, little known about biochemical properties. By combining bioluminescence...
Mitochondrial dysfunction is an early, imminent event in neurodegenerative disorders including Parkinson disease (PD) and Alzheimer (AD). The enzymatic pair PINK1 PRKN/Parkin recognize transiently label damaged mitochondria with ubiquitin (Ub) phosphorylated at Ser65 (p-S65-Ub) as a signal for degradation via the autophagy-lysosome system (mitophagy). Despite its discovery cell culture several years ago, robust quantitative detection of altered mitophagy vivo has remained challenging. Here...
Background: Parkinson's disease (PD) is a progressive neurodegenerative disorder. Mendelian forms have revealed multiple genes, with notable emphasis on membrane trafficking; RAB GTPases play an important role in PD as subset are both regulators and substrates of LRRK2 kinase. To explore the PD, we undertook comprehensive examination their genetic variability familial PD.Methods: Affected probands from 130 multi-incident families underwent whole-exome sequencing genotyping, Potential...
Loss-of-function mutations in PINK1 are causally linked to recessively inherited Parkinson's disease (PD), with marked loss of dopaminergic neurons the substantia nigra that required for normal movement. is a nuclear-encoded mitochondrial-targeted kinase phosphorylates conserved serine at amino acid 65 (pS65) ubiquitin as well Parkin, another gene loss-of-function recessive parkinsonism. The steady-state levels protein very low, even cells express PINK1, because normally targeted degradation...
Summary Background Parkinson’s disease (PD) is a progressive neurodegenerative disorder. Mendelian forms have revealed multiple genes, with notable emphasis on membrane trafficking; RAB GTPases play an important role in PD as subset are both regulators and substrates of LRRK2 protein kinase. To explore the PD, we undertook comprehensive examination their genetic variability familial PD. Methods Affected probands from 130 multi-incident families underwent whole-exome sequencing genotyping,...
Previous studies have shown that dopamine and galanin modulate cholinergic transmission in the hippocampus, but little is known about mechanisms involved their possible interactions. By using resonance energy transfer techniques transfected mammalian cells, we demonstrated existence of heteromers between D 1 -like receptors (D 5 ) Gal , not 2 receptors. Within –Gal receptor heteromers, activation potentiated blockade counteracted MAPK induced by stimulation receptors, whereas or did modify...
Abstract Genetic and neuropathological evidence strongly implicates aberrant forms of α-synuclein in neurodegeneration. Antibodies specific for phosphorylated at serine 129 (pS129) are selective the pathological protein aggregates that characteristic Parkinson’s disease (PD) other synucleinopathies, such as dementia with Lewy bodies (DLB) multiple system atrophy (MSA). Although etiology most synucleinopathies remains uncertain, a large body points to mitochondrial dysfunction. The recent...
Neurodegeneration is an age-dependent progressive phenomenon with no defined cause. Aging the main risk factor for neurodegenerative diseases. During aging, activated microglia undergoes phenotypic alterations that can lead to neuroinflammation, which well accepted event in pathogenesis of Several common mechanisms are shared by genetically or pathologically distinct diseases, such as excitotoxicity, mitochondrial deficits and oxidative stress, protein misfolding translational dysfunction,...
Increased oxidative stress has been implicated in the pathogenesis of dopaminergic neurodegeneration leading to development Parkinson's disease. In this study, we investigated whether naphtha[1,2-d]thiazol-2-amine (NTA) may ameliorate haloperidol-induced catalepsy and damage mice brain. Haloperidol-induced was measured with standard bar test. The extent evaluated by measuring levels MDA, GSH activities antioxidant enzymes (SOD GSH-Px) from brain homogenate. Haloperidol treatment...
BACE1 is a key enzyme facilitating the generation of neurotoxic β-amyloid (Aβ) peptide. However, given that has multiple substrates we explored importance in maintenance retinal pigment epithelial (RPE) cell homeostasis under oxidative stress. Inhibition reduced mitochondrial membrane potential, increased fragmentation, and cleaved caspase-3 expression cells inhibition also resulted significantly lower levels fusion proteins OPA1 MFN1 suggesting higher rate fission while increasing...
This study investigated the therapeutic potential of nuclear retinoid X receptor (RXR) in mitigating progression alpha-synucleinopathies (αSNPs), particularly Parkinson's disease (PD). PD-like pathology mice was successfully induced through co-delivery AAV expressing human α-synuclein (αS) and αS preformed fibrils (PFFs) into substantia nigra pars compacta (SNpc). Significant increases Lewy body (LB)-like inclusions, loss tyrosine hydroxylase-positive (TH+) neurons, reductions dopamine (DA)...