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Related Concept Videos

Parkinson's Disease: Overview01:15

Parkinson's Disease: Overview

Neurodegenerative disorders are progressive diseases that cause irreversible damage and loss to neurons in specific brain areas. Examples of these disorders include Parkinson's disease, Alzheimer's disease, Multiple Sclerosis (MS), and Amyotrophic Lateral Sclerosis (ALS). These disorders share characteristics such as proteinopathies, selective neuronal vulnerability, and a complex interplay between genetic and environmental factors. The primary therapeutic goal for these conditions is to...
Parkinson Disease l: Introduction01:24

Parkinson Disease l: Introduction

Parkinson’s disease is a chronic, progressive neurodegenerative disorder that primarily affects movement. It is characterized by motor symptoms such as resting tremors, muscle rigidity, bradykinesia (slowness of movement), and postural instability. Patients may notice hand tremors at rest, stiffness during movement, or a shuffling gait. In addition to motor features, non-motor symptoms include sleep disturbances, mood and behavioral changes, constipation, and cognitive impairment, all of which...
Parkinson's Disease: Treatment01:24

Parkinson's Disease: Treatment

Neurodegenerative disorders, such as Parkinson's Disease (PD), involve the gradual and irreversible destruction of neurons in particular brain areas. These disorders exhibit standard features like proteinopathies, selective vulnerability of some neurons, and an interaction of intrinsic properties, genetics, and environmental influences in neural injury.
Parkinson's Disease is primarily a result of the loss of dopaminergic neurons in the substantia nigra pars compacta. The cornerstone of its...
Parkinson Disease ll: Pathophysiology01:24

Parkinson Disease ll: Pathophysiology

Parkinson disease (PD) is a progressive neurodegenerative disorder primarily affecting movement, with additional non-motor features. Its pathophysiology involves complex interactions among genetic susceptibility, environmental exposures, and cellular dysfunction, including dopaminergic neuron loss, protein aggregation, and mitochondrial impairment.Selective NeurodegenerationA key feature is the degeneration of dopaminergic neurons in the substantia nigra pars compacta, leading to reduced...
Alterations in Muscle Tone lll01:11

Alterations in Muscle Tone lll

Rigidity and myotonia are distinct abnormalities of muscle tone that affect resistance and relaxation during movement. Although both involve altered muscle contraction, they arise from different neurological and muscular mechanisms.CharacteristicsRigidity is characterized by uniform resistance to passive movement across the entire range, independent of speed, affecting flexors and extensors equally. It may appear as lead-pipe rigidity (smooth, constant resistance) or cogwheel rigidity...
Alterations in Muscle Tone ll01:12

Alterations in Muscle Tone ll

Alterations in muscle tone are common manifestations of neurological disorders and reflect dysfunction within different nervous system regions. Spasticity, paratonia, and dystonia represent distinct forms of hypertonia, each with unique mechanisms, clinical features, and diagnostic importance.CharacteristicsSpasticity happens from upper motor neuron lesions and is characterized by velocity-dependent resistance to passive movement. Clinical features include:Exaggerated deep tendon reflexesClonus...

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Related Experiment Video

Updated: May 10, 2026

Rating L-DOPA-Induced Dyskinesias in the Unilaterally 6-OHDA-Lesioned Rat Model of Parkinson's Disease
06:45

Rating L-DOPA-Induced Dyskinesias in the Unilaterally 6-OHDA-Lesioned Rat Model of Parkinson's Disease

Published on: October 4, 2021

Atypical parkinsonism: an update.

Maria Stamelou1, Guenter U Hoeglinger

  • 1Sobell Department for Motor Neurosciences and Movement Disorders, UCL Institute of Neurology, Queen Square, London, UK. m.stamelou@ucl.ac.uk

Current Opinion in Neurology
|July 2, 2013
PubMed
Summary

Recent advances in atypical parkinsonism reveal new genetic factors and diagnostic criteria. However, the lack of effective biomarkers hinders the development of successful treatments for these challenging neurodegenerative disorders.

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Induction and Assessment of Levodopa-induced Dyskinesias in a Rat Model of Parkinson's Disease
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Related Experiment Videos

Last Updated: May 10, 2026

Rating L-DOPA-Induced Dyskinesias in the Unilaterally 6-OHDA-Lesioned Rat Model of Parkinson's Disease
06:45

Rating L-DOPA-Induced Dyskinesias in the Unilaterally 6-OHDA-Lesioned Rat Model of Parkinson's Disease

Published on: October 4, 2021

Induction and Assessment of Levodopa-induced Dyskinesias in a Rat Model of Parkinson's Disease
05:51

Induction and Assessment of Levodopa-induced Dyskinesias in a Rat Model of Parkinson's Disease

Published on: October 14, 2021

Area of Science:

  • Neuroscience
  • Genetics
  • Neurology

Background:

  • Atypical parkinsonism encompasses a group of neurodegenerative disorders with overlapping symptoms but distinct pathologies.
  • Progressive supranuclear palsy and corticobasal degeneration are key conditions within this spectrum.
  • Current understanding of their genetic underpinnings and diagnostic markers remains incomplete.

Purpose of the Study:

  • To review recent advancements in the genetics, diagnosis, and treatment of atypical parkinsonism.
  • To highlight the challenges and future directions in the field.

Main Methods:

  • Literature review of studies published in the last two years.
  • Analysis of findings from genome-wide association studies.
  • Evaluation of revised diagnostic criteria and emerging biomarker research.

Main Results:

  • Identification of novel genetic risk factors for progressive supranuclear palsy.
  • Description of new genetic conditions associated with atypical parkinsonism.
  • Revision of diagnostic criteria for corticobasal degeneration and progressive supranuclear palsy.
  • Preliminary but promising research into molecular biomarkers.
  • Failure of recent therapeutic trials targeting disease-specific pathways.

Conclusions:

  • Significant deficits persist in understanding and treating atypical parkinsonism.
  • The expanding phenotypic spectrum complicates early patient identification.
  • The absence of validated biomarkers is the primary obstacle to developing effective treatments.
  • Future research must prioritize biomarker discovery to enable therapeutic advancements.