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Related Concept Videos

Amyloid Fibrils03:03

Amyloid Fibrils

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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,...
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Amyloid Fibrils03:03

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Alzheimer Disease ll: Pathophysiology01:23

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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...
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Parkinson Disease ll: Pathophysiology01:24

Parkinson Disease ll: Pathophysiology

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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...
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Alzheimer Disease l: Introduction01:29

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Alzheimer disease is a chronic, progressive, and irreversible neurodegenerative disorder and the most common cause of dementia in older adults. It leads to gradual neuronal loss, causing cognitive decline, behavioral changes, and loss of functional independence.Risk Factors and EtiologyThe disease is multifactorial. Age is the strongest risk factor, with prevalence doubling every 5 years after age 65. Genetic factors include mutations in genes such as APP, PSEN1, and PSEN2, which are associated...
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Related Experiment Video

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Monitoring Cell-to-cell Transmission of Prion-like Protein Aggregates in Drosophila Melanogaster
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[Amyloidgenesis in prion disease].

Yoshio Tsuboi1

  • 1Department of Neurology, Fukuoka University Faculty of Medicine.

Brain and Nerve = Shinkei Kenkyu No Shinpo
|July 8, 2014
PubMed
Summary

Prion diseases are fatal neurodegenerative disorders caused by misfolded prion proteins (PrPSc). This study examines these conditions as a form of localized brain amyloidosis.

Area of Science:

  • Neuroscience
  • Protein misfolding diseases
  • Neurodegenerative disorders

Context:

  • Prion diseases, or transmissible spongiform encephalopathies, affect humans and mammals.
  • Pathogenesis involves the conversion of normal prion protein (PrPC) to abnormal PrPSc.
  • PrPSc accumulation in the brain leads to spongiform change, gliosis, and neuronal loss.

Purpose:

  • To discuss prion diseases through the lens of localized amyloidosis.
  • To highlight the amyloidogenic nature of the prion protein.

Summary:

  • Prion diseases are characterized by the conformational change of PrPC to PrPSc.
  • PrPSc is β-sheet rich, proteinase-resistant, and accumulates in the brain.
  • These protein aggregates are linked to the neuropathology observed in prion diseases.

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Screening for Amyloid Aggregation by Semi-Denaturing Detergent-Agarose Gel Electrophoresis
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Investigating the Spreading and Toxicity of Prion-like Proteins Using the Metazoan Model Organism C. elegans
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Screening for Amyloid Aggregation by Semi-Denaturing Detergent-Agarose Gel Electrophoresis
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Impact:

  • Provides a novel perspective on prion disease pathogenesis.
  • Connects prion diseases to the broader field of amyloidosis research.
  • Enhances understanding of neurodegenerative mechanisms.