Evidence map›Paper›PMID 34817799›Full record

ArticleNeurotoxicity research2022

Intranasal Exposure to Low-Dose Rotenone Induced Alpha-Synuclein Accumulation and Parkinson's Like Symptoms Without Loss of Dopaminergic Neurons.

Monika Sharma, Jaswinder Kaur, Siddhi Rakshe, Nishant Sharma, Dignesh Khunt, Amit Khairnar

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In one paragraph

Article in Neurotoxicity research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 17% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Pooled it
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  4. Research Priorities on the Role of α-Synuclein in Parkinson's Disease Pathogenesis.Movement disorders : official journal of the Movement Disorder Society · 2024
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Monika SharmaDepartment of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER), Ahmedabad, Opposite Air Force Station, Palaj, Gandhinagar, Gujarat, 382355, India.
Jaswinder Kaur *Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER), Ahmedabad, Opposite Air Force Station, Palaj, Gandhinagar, Gujarat, 382355, India.
Siddhi Rakshe *Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER), Ahmedabad, Opposite Air Force Station, Palaj, Gandhinagar, Gujarat, 382355, India.
Nishant SharmaDepartment of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER), Ahmedabad, Opposite Air Force Station, Palaj, Gandhinagar, Gujarat, 382355, India.
Dignesh KhuntDepartment of Pharmaceutics, National Institute of Pharmaceutical Education and Research (NIPER), Ahmedabad, Opposite Air Force Station, Gandhinagar, Gujarat, 382355, India.
Amit KhairnarDepartment of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER), Ahmedabad, Opposite Air Force Station, Palaj, Gandhinagar, Gujarat, 382355, India. amitk@niperahm.res.in.ORCID http://orcid.org/0000-0003-3375-774X
National Institute of Pharmaceutical Education and Research (NIPER) - Ahmedabad · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epidemiologically Parkinson's disease (PD) is associated with chronic ingestion or inhalation of environmental toxins leading to the development of motor symptoms. Though neurotoxin-based animal models played a major role in understanding diverse pathogenesis, they failed to identify the risk assessment due to uncommon route of toxin exposure. Towards this, the available neurotoxin-based intranasal (i.n.) PD models targeting olfactory bulb (OB) have demonstrated the dopaminergic (DAergic) neurodegeneration in both OB and substantia nigra (SN). Despite that, the studies detecting the alpha-synuclein (α-syn) accumulation in OB and its progression to other brain regions due to inhalation of environmental toxins are still lacking. Herein, we developed oil in water microemulsion of rotenone administered intranasally to the mice at a dose which is not detectable in blood, brain, and olfactory bulb by LCMS method. Our data reveals that 9 weeks of rotenone exposure did not induce olfactory and motor dysfunction. Conversely, after 16 weeks of washout period, rotenone treated mice showed both olfactory and motor impairment, along with α-syn accumulation in the OB and striatum without glial cell activation and loss of dopaminergic neurons. The results depict the progressive nature of the developed model and highlight the role of α-syn in PD like pathology or symptoms. Together, our findings suggest the adverse consequences of early exposure to the environmental toxins on the olfactory system for a shorter period with relevance to the development of synucleinopathy or Parkinson's disease in its later stage.

Indexed as

alpha-SynucleinParkinson DiseaseAnimalsDisease Models, AnimalDopaminergic NeuronsMiceRotenoneSubstantia Nigraalpha-SynucleinRotenoneAlpha-synucleinDopaminergic neurodegenerationIntranasalOlfactory bulbParkinson’s diseasePhosphorylated alpha-synucleinRotenone

Identifiers

PMID34817799
OpenAlexW3217684053

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.