We are analyzing https://link.springer.com/article/10.1602/neurorx.1.1.139.

Title:
Neurodegeneration and neuroprotection in Parkinson disease | Neurotherapeutics
Description:
Many of the motoric features that define Parkinson disease (PD) result primarily from the loss of the neuromelanin (NM)-containing dopamine (DA) neurons of the substantia nigra (SN), and to a lesser extent, other mostly catecholaminergic neurons, and are associated with cytoplasmic “Lewy body” inclusions in some of the surviving neurons. While there are uncommon instances of familial PD, and rare instances of known genetic causes, the etiology of the vast majority of PD cases remains unknown (i.e., idiopathic). Here we outline genetic and environmental findings related to PD epidemiology, suggestions that aberrant protein degradation may play a role in disease pathogenesis, and pathogenetic mechanisms including oxidative stress due to DA oxidation that could underlie the selectivity of neurodegeneration. We then outline potential approaches to neuroprotection for PD that are derived from current notions on disease pathogenesis.
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Keywords {🔍}

google, scholar, pubmed, cas, parkinsons, disease, dopamine, neurol, alphasynuclein, neurosci, neurons, sulzer, parkinson, parkinsonism, sci, fahn, acad, chem, res, med, lee, neurochem, natl, usa, biol, parkin, article, neurodegeneration, study, chronic, dopaminergic, human, cell, synaptic, brain, mptp, neurotrophic, engl, model, liu, neurotoxicity, neuroprotection, role, disord, diseasej, implications, effect, midbrain, gene, effects,

Topics {✒️}

[123i]fp-cit spect e2-dependent ubiquitin-protein ligase double-blind placebo-controlled study parkinsonism-inducing drug 1-methyl-4-phenylpyridinium oxidative post-translational modifications display neurotrophic activity glutathione-protein-mixed disulfides alpha-synuclein locus triplication cytoplasmic alpha-synuclein aggregates glialderived neurotrophic factor ubiquitin-dependent degradation system randomized placebo-controlled extension alpha-synuclein gene identified dopamine-alpha-synuclein adduct mice lacking alpha-synuclein methionine-oxidized alpha-synuclein gene encoding alpha-synuclein neuron-specific protein localized metabolite n-methyl-4-phenylpyridine intraneuronal dopamine-quinone synthesis autophagic cell death vesicular monoamine transporters vesicular monoamine transporter privacy choices/manage cookies alpha-synuclein regulates induced cell damage brain mitochondrial respiration levodopa-treated parkinson secretory vesicle ph intraparenchymal putaminal administration nigrostriatal dopamine system striatal dopamine deficiency drug-induced parkinsonism ubiquitin ligase complex vesicular amine transporter striatal dopamine loss environmental findings related intracellular nitrative insult nf-κb dependent brain dopamine depletion dopamine-induced toxicity midbrain dopaminergic neurons dopaminergic neurons occurs dopaminergic midbrain neurons ilsa working group parkin gene leads activating glutathione system chronic manganese poisoning chronic manganese intoxication ubiquitin pathway

Questions {❓}

The cell biology of alpha-synuclein: a sticky problem?

Schema {🗺️}

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         description:Many of the motoric features that define Parkinson disease (PD) result primarily from the loss of the neuromelanin (NM)-containing dopamine (DA) neurons of the substantia nigra (SN), and to a lesser extent, other mostly catecholaminergic neurons, and are associated with cytoplasmic “Lewy body” inclusions in some of the surviving neurons. While there are uncommon instances of familial PD, and rare instances of known genetic causes, the etiology of the vast majority of PD cases remains unknown (i.e., idiopathic). Here we outline genetic and environmental findings related to PD epidemiology, suggestions that aberrant protein degradation may play a role in disease pathogenesis, and pathogenetic mechanisms including oxidative stress due to DA oxidation that could underlie the selectivity of neurodegeneration. We then outline potential approaches to neuroprotection for PD that are derived from current notions on disease pathogenesis.
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