Evidence map›Paper›PMID 30267336›Full record

ReviewNeurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology2019

Understanding multifactorial architecture of Parkinson's disease: pathophysiology to management.

Ramandeep Kaur, Sidharth Mehan, Shamsher Singh

Abstract readReview
PubMed Publisher
In one paragraph

Review in Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 4 pooled it
6.5field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

55 citing papers in PubMed, 4 syntheses or guidelines pooled it, 109 citations in OpenAlex.

  1. Pooled it
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  3. Suicide and suicide attempts after subthalamic nucleus stimulation in Parkinson's disease: a systematic review and meta-analysis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2021
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  10. Preclinical Evaluation ofMolecules (Basel, Switzerland) · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Ramandeep KaurNeuroscience Division, Department of Pharmacology, Indo-Soviet Friendship College of Pharmacy, Moga, Punjab, India.
Sidharth MehanNeuroscience Division, Department of Pharmacology, Indo-Soviet Friendship College of Pharmacy, Moga, Punjab, India.
Shamsher SinghNeuroscience Division, Department of Pharmacology, Indo-Soviet Friendship College of Pharmacy, Moga, Punjab, India. shamshersinghbajwa@gmail.com.ORCID http://orcid.org/0000-0002-2780-6632
Indo Soviet Friendship College of Pharmacy · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's disease (PD) is the second most common multifactorial neurodegenerative disorder affecting 3% of population during elder age. The loss of substantia nigra, pars compacta (SNpc) neurons and deficiency of striatal dopaminergic neurons produces stables motor deficient. Further, increase alpha-synuclein accumulation, mitochondrial dysfunction, oxidative stress, excitotoxicity, and neuroinflammation plays a crucial role in the pathogenesis of PD. Alpha-synuclein protein encodes for SNCA gene and disturbs the normal physiological neuronal signaling via altering mitochondrial homeostasis. The level of α-synuclein is increased in both normal aging and PD brain to a greater extent and secondly reduced clearance results in accumulation of Lewy bodies (LB). Emerging evidences indicate that mitochondrial dysfunction might be a common cause but pathological insult through protein misfolding, aggregation, and accumulation leads to neuronal apoptosis. The observation supporting that expression of DJ-1, LLRK2, PARKIN, PINK1, and excessive excitotoxicity mediated by dysbalance between GABA and glutamate reduced mitochondrial functioning and increased neurotoxicity. Therefore, the present review summarizes the various pathological mechanisms and also explores the therapeutic strategies which could be useful to ameliorate movement disorder like Parkinsonism.

Indexed as

Disease Managementalpha-SynucleinAnimalsDopaminergic NeuronsHumansMitochondriaOxidative StressParkinson DiseaseUbiquitin-Protein Ligasesalpha-Synucleinparkin proteinUbiquitin-Protein LigasesDopaminergic neuronsNeurotransmittersParkinson diseaseSubstantia nigra pars compacta

Identifiers

PMID30267336
OpenAlexW2892711299

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.