Evidence map›Paper›PMID 27790086›Full record

ArticleFrontiers in neuroscience2016

Traumatic Brain Injury Leads to Development of Parkinson's Disease Related Pathology in Mice.

Daniela Impellizzeri, Michela Campolo, Giuseppe Bruschetta, Rosalia Crupi, Marika Cordaro, Irene Paterniti, Salvatore Cuzzocrea, Emanuela Esposito

Open access · goldAbstract read
In one paragraph

Article in Frontiers in neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
5.4field-weighted citation impact, top 4% 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

52 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.

  1. Pooled it
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  3. Benzoate Drugs for Traumatic Brain Injury.Journal of clinical & experimental immunology · 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

8 authors at 1 institution in 2 countries.

Daniela ImpellizzeriDepartment of Chemical, Biological, Pharmaceutical, and Environmental Sciences, University of Messina Messina, Italy.
Michela CampoloDepartment of Chemical, Biological, Pharmaceutical, and Environmental Sciences, University of Messina Messina, Italy.
Giuseppe BruschettaDepartment of Chemical, Biological, Pharmaceutical, and Environmental Sciences, University of Messina Messina, Italy.
Rosalia CrupiDepartment of Chemical, Biological, Pharmaceutical, and Environmental Sciences, University of Messina Messina, Italy.
Marika CordaroDepartment of Chemical, Biological, Pharmaceutical, and Environmental Sciences, University of Messina Messina, Italy.
Irene PaternitiDepartment of Chemical, Biological, Pharmaceutical, and Environmental Sciences, University of Messina Messina, Italy.
Salvatore CuzzocreaDepartment of Chemical, Biological, Pharmaceutical, and Environmental Sciences, University of MessinaMessina, Italy; Department of Pharmacology and Physiology, Saint Louis UniversitySt. Louis, MO, USA.
Emanuela EspositoDepartment of Chemical, Biological, Pharmaceutical, and Environmental Sciences, University of Messina Messina, Italy.
University of Messina · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Traumatic brain injury (TBI) is a major health and socio-economic problem that affects all societies. This condition results from the application of external physical strength to the brain that leads to transitory or permanent structural and functional impairments. Moreover, TBI is a risk factor for neurodegeneration and can e.g., increase the risk for Parkinson's disease (PD), a late-onset neurodegenerative disorder with loss of dopaminergic neurons in substantia nigra. In this study, we wanted to explore the possible development of PD-related pathology within the context of an experimental model of TBI. Traumatic brain injury was induced in mice by controlled cortical impact. At different time points behavioral tests (open field, elevated plus maze tests, and Barnes maze) were performed: The animals were sacrificed 30 days after the impact and the brains were processed for Western blot and immunohistochemical analyses. Following TBI there was a significant decrease in expression of tyrosine hydroxylase and dopamine transporter in the substantia nigra as well as significant behavioral alterations. In addition, a strong increase in neuroinflammation was evident, as shown by increased levels of cyclooxygenase-2 and inducible nitric oxide synthase as well as IκB-α degradation and nuclear-κB translocation. Moreover, neurotrophic factors such as brain-derived neurotrophic factor, neurotrophin-3, nerve growth factor, and glial cell line-derived neurotrophic factor were decreased 30 days post-TBI. Interestingly, we observed a significant accumulation of α-synuclein in microglia compared to astrocytes. This study suggests that PD-related molecular events can be triggered upon TBI. The biological mechanisms linking brain trauma and neurodegenerative diseases need to be further investigated.

Indexed as

astrocyteschronic traumatic brain injurymicroglianeurotrophic factorsnon-motor symptomsnuclear factor-κBParkinson's diseaseα-synuclein

Identifiers

PMID27790086
PMCPMC5061819
OpenAlexW2530961952

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.