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Related Concept Videos

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...
Amyloid Fibrils03:03

Amyloid Fibrils

Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
Amyloid deposits were observed as early as 1639 in the liver and the spleen.   In 1854, Rudolph Virchow performed iodine staining, normally used to...
Amyloid Fibrils03:03

Amyloid Fibrils

Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
Amyloid deposits were observed as early as 1639 in the liver and the spleen.   In 1854, Rudolph Virchow performed iodine staining, normally used to...
Alzheimer Disease ll: Pathophysiology01:23

Alzheimer Disease ll: Pathophysiology

Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...

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Related Experiment Video

Updated: May 26, 2026

Exogenous Administration of Microsomes-associated Alpha-synuclein Aggregates to Primary Neurons As a Powerful Cell Model of Fibrils Formation
09:16

Exogenous Administration of Microsomes-associated Alpha-synuclein Aggregates to Primary Neurons As a Powerful Cell Model of Fibrils Formation

Published on: June 26, 2018

Synucleinopathies from bench to bedside.

Andreas Puschmann1, Roongroj Bhidayasiri, William J Weiner

  • 1Department for Geriatric Psychiatry, Lund University, Sweden. andreas.puschmann@med.lu.se

Parkinsonism & Related Disorders
|December 15, 2011
PubMed
Summary
This summary is machine-generated.

Alpha-synuclein accumulation defines synucleinopathies like Parkinson

More Related Videos

Studying Pre-formed Fibril Induced α-Synuclein Accumulation in Primary Embryonic Mouse Midbrain Dopamine Neurons
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Studying Pre-formed Fibril Induced α-Synuclein Accumulation in Primary Embryonic Mouse Midbrain Dopamine Neurons

Published on: August 16, 2020

Sequential Extraction of Soluble and Insoluble Alpha-Synuclein from Parkinsonian Brains
09:27

Sequential Extraction of Soluble and Insoluble Alpha-Synuclein from Parkinsonian Brains

Published on: January 5, 2016

Related Experiment Videos

Last Updated: May 26, 2026

Exogenous Administration of Microsomes-associated Alpha-synuclein Aggregates to Primary Neurons As a Powerful Cell Model of Fibrils Formation
09:16

Exogenous Administration of Microsomes-associated Alpha-synuclein Aggregates to Primary Neurons As a Powerful Cell Model of Fibrils Formation

Published on: June 26, 2018

Studying Pre-formed Fibril Induced α-Synuclein Accumulation in Primary Embryonic Mouse Midbrain Dopamine Neurons
10:03

Studying Pre-formed Fibril Induced α-Synuclein Accumulation in Primary Embryonic Mouse Midbrain Dopamine Neurons

Published on: August 16, 2020

Sequential Extraction of Soluble and Insoluble Alpha-Synuclein from Parkinsonian Brains
09:27

Sequential Extraction of Soluble and Insoluble Alpha-Synuclein from Parkinsonian Brains

Published on: January 5, 2016

Area of Science:

  • Neurology
  • Molecular Pathology

Background:

  • Alpha-synuclein aggregation is a hallmark of neurodegenerative diseases.
  • Diseases are being reclassified based on alpha-synuclein pathology, including Parkinson's disease (PD), dementia with Lewy bodies (DLB), Parkinson's disease dementia (PDD), and multiple system atrophy (MSA).
  • Conditions like Attention-Deficit/Hyperactivity Disorder (ADHD) and Restless Legs Syndrome (RLS) may share underlying dopaminergic dysregulation or genetic links with synucleinopathies.

Purpose of the Study:

  • To review the clinical features of alpha-synucleinopathies.
  • To differentiate synucleinopathies from conditions with similar symptoms but different pathologies.
  • To highlight the potential of targeting alpha-synuclein for novel therapeutic strategies.

Main Methods:

  • Literature review and synthesis of current research on alpha-synuclein.
  • Analysis of clinical presentations and pathological findings across various neurological disorders.
  • Discussion of emerging therapeutic approaches targeting alpha-synuclein.

Main Results:

  • Alpha-synuclein pathology is present in PD, DLB, PDD, MSA, and some cases of Essential Tremor (ET) and lysosomal storage disorders.
  • Non-fibrillar oligomers of alpha-synuclein may represent the toxic species, with Lewy body formation potentially being a protective mechanism.
  • Early symptoms like ADHD or personality changes can precede the overt diagnosis of synucleinopathies.

Conclusions:

  • Accurate clinical differentiation of synucleinopathies is crucial for effective management and treatment.
  • Targeting alpha-synuclein toxicity presents a promising therapeutic avenue for these neurodegenerative diseases.
  • Understanding the spectrum of alpha-synuclein-related disorders is essential for future clinical practice.