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Related Concept Videos

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...
Subviral Agents01:29

Subviral Agents

Subviral agents are infectious entities that resemble viruses but lack one or more viral components, such as a capsid or essential replication machinery. These agents include viroids, prions, and satellites, each possessing distinct structural and functional characteristics that influence their mode of infection and replication.Viroids are the simplest subviral agents, consisting of circular, single-stranded RNA molecules without a protein coat. They exclusively infect plants, relying entirely...
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...
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...
Viral Recombination00:57

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Cells are sometimes infected by more than one virus at once. When two viruses disassemble to expose their genomes for replication in the same cell, similar regions of their genomes can pair together and exchange sequences in a process called recombination. Alternatively, viruses with segmented genomes can swap segments in a process called reassortment.

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Prion Safety Laboratory Swipe Test
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[Acquired human prion diseases--past and present issues].

Ken'ichi Hagiwara1, Yoshio Yamakawa, Kentaro Hanada

  • 1Department of Biochemistry and Cell Biology, National Institute of Infectious Diseases, 1-23-1 Toyama, Shinjuku-ku, Tokyo 162-8640, Japan. hagiwark@nih.go.jp

Uirusu
|March 12, 2010
PubMed
Summary

Transmissible spongiform encephalopathies, or prion diseases, are fatal neurodegenerative conditions. Variant Creutzfeldt-Jakob disease (vCJD) prions accumulate in lymphoid tissues, raising concerns about blood transfusion safety.

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Published on: January 8, 2015

Area of Science:

  • Neuroscience
  • Infectious Diseases
  • Pathology

Context:

  • Transmissible spongiform encephalopathies (TSEs), or prion diseases, are fatal neurodegenerative disorders.
  • Human prion diseases are classified into sporadic, inherited, and acquired forms.
  • Sporadic Creutzfeldt-Jakob disease (CJD) accounts for 80-90% of human prion diseases.

Purpose:

  • To review past and present issues concerning acquired human prion diseases.
  • To highlight the characteristics of variant CJD (vCJD) and its implications.
  • To discuss the potential for transfusion-mediated transmission of vCJD.

Summary:

  • Prion diseases involve the accumulation of abnormal prion protein (PrPSc) in the central nervous system.
  • Variant CJD (vCJD), acquired through ingestion of BSE prion, differs from sporadic CJD in PrPSc distribution.
  • vCJD cases show PrPSc accumulation in spleen and tonsils, unlike sporadic CJD.

Impact:

  • The distribution of PrPSc in lymphoid tissues in vCJD raises concerns about blood and blood product infectivity.
  • Five probable cases of transfusion-mediated vCJD transmission have been reported in the UK.
  • Understanding acquired prion diseases is crucial for public health and transfusion safety protocols.