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Related Experiment Video

Updated: Jul 3, 2026

The Use of Primary Human Fibroblasts for Monitoring Mitochondrial Phenotypes in the Field of Parkinson's Disease

The Use of Primary Human Fibroblasts for Monitoring Mitochondrial Phenotypes in the Field of Parkinson's Disease

Published on: October 3, 2012

Parkinson's disease: genetics and beyond.

N N Inamdar¹, D K Arulmozhi, A Tandon

¹Allana College of Pharmacy, Azam Campus, Camp. Pune 411 001, India.

Current Neuropharmacology

|July 11, 2008

Summary

This summary is machine-generated.

Parkinson's disease (PD) involves dopamine neuron loss and Lewy bodies. Research reviews genetic and environmental factors, mitochondrial dysfunction, and protein aggregation contributing to PD's complex pathophysiology.

Keywords:

Mitochondrial dysfunction Parkin Parkinson’s disease lewy bodies pathophysiology protein aggregation α-Synuclein

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Gene-environment Interaction Models to Unmask Susceptibility Mechanisms in Parkinson's Disease

Gene-environment Interaction Models to Unmask Susceptibility Mechanisms in Parkinson's Disease

Published on: January 7, 2014

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Last Updated: Jul 3, 2026

The Use of Primary Human Fibroblasts for Monitoring Mitochondrial Phenotypes in the Field of Parkinson's Disease

The Use of Primary Human Fibroblasts for Monitoring Mitochondrial Phenotypes in the Field of Parkinson's Disease

Published on: October 3, 2012

Gene-environment Interaction Models to Unmask Susceptibility Mechanisms in Parkinson's Disease

Gene-environment Interaction Models to Unmask Susceptibility Mechanisms in Parkinson's Disease

Published on: January 7, 2014

Area of Science:

Neuroscience
Pathology
Genetics

Background:

Parkinson's disease (PD) is a neurodegenerative disorder marked by motor symptoms like tremor and rigidity.
It results from selective loss of dopamine neurons in the substantia nigra, accompanied by Lewy bodies.

Purpose of the Study:

To review evidence linking various factors to Parkinson's disease pathophysiology.
To discuss candidate genes, proteins, and therapeutic strategies for PD.

Main Methods:

Review of diverse scientific evidence.
Critical discussion of current and future pharmacotherapies for PD.

Main Results:

Implicated factors include mitochondrial complex I dysfunction, altered redox state, proapoptotic factors, and ubiquitin-proteasome pathway dysfunction.
Genetic aberrations, environmental toxins, and abnormal protein aggregation are hypothesized to cause neurodegeneration.

Conclusions:

The exact pathoetiology of cell death in PD is complex and multifactorial.
Understanding these factors is crucial for developing effective therapeutic strategies for Parkinson's disease.