Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Modulation of mitochondrial phenotypes by endurance exercise contributes to neuroprotection against a MPTP-induced animal model of PD.

Life sciences - 15 Sept 2018

Jang Yongchul, Kwon Insu, Song Wankeun, Cosio-Lima Ludmila M, Taylor Scott, Lee Youngil

Abstract excerpt

AIM: Endurance exercise (EE) has been reported to confer neuroprotection against Parkinson's disease (PD); however, underlying molecular mechanisms of the protection remain still unclear. Since mitochondrial impairment is commonly observed in the brain of PD patients and animals, this study investigated whether EE-induced neuroprotection is associated with mitochondrial phenotypes, using a mouse model of PD...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Apoptosis
Share to Exercise Therapy

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Mitochondria

Share to Neuroblastoma

Share to Neuroprotection

Share to Neurotoxins

Share to Parkinson Disease

Share to Tumor Cells, Cultured

Source

Identifiers

PMID: 30144449
DOI: 10.1016/j.lfs.2018.08.045

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Modulation of mitochondrial phenotypes by endurance exercise contributes to neuroprotection against a MPTP-induced animal model of PD.PMID 30144449Read ↗

Physical exercise may exert its therapeutic influence on Alzheimer's disease through the reversal of mitochondrial dysfunction via SIRT1–FOXO1/3–PINK1–Parkin-mediated mitophagySemantic proximity Read ↗

Endoplasmic Reticulum Stress Inhibition Promotes Mitophagy via Miro1 Reduction to Rescue Mitochondrial Dysfunction and Protect Dopamine Neurons in Parkinson’s DiseaseSemantic proximity Read ↗

Mitochondrial Effects of PGC-1alpha Silencing in MPP+ Treated Human SH-SY5Y Neuroblastoma CellsSemantic proximity Read ↗

Testosterone ameliorates age-related brain mitochondrial dysfunctionSemantic proximity Read ↗

Mitochondria and Programmed Cell Death in Parkinson's Disease: Apoptosis and BeyondSemantic proximity Read ↗

Ergothioneine Treatment Ameliorates the Pathological Phenotypes of Parkinson's Disease ModelsSemantic proximity Read ↗

Exercise does not protect against MPTP-induced neurotoxicity in BDNF haploinsufficient mice.Semantic proximity Read ↗

Apoptotic factors and mitochondrial complexes assist determination of strain-specific susceptibility of mice to Parkinsonian neurotoxin MPTPSemantic proximity Read ↗

Forced exercise activates the NrF2 pathway in the striatum and ameliorates motor and behavioral manifestations of Parkinson's disease in rotenone-treated ratsSemantic proximity Read ↗

Piperine Enhances Mitochondrial Biogenesis to Mitigate Stress in SH ‐ SY5Y Neuroblastoma CellsSemantic proximity Read ↗

Cerebroventricular Microinjections of MPTP on Adult Zebrafish Induces Dopaminergic Neuronal Death, Mitochondrial Fragmentation, and Sensorimotor ImpairmentsSemantic proximity Read ↗

Neuroprotection and dopamine agonistsSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.