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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...
Lysosomal Hydrolases01:22

Lysosomal Hydrolases

Lysosomes are the site for the degradation of macromolecules and biological polymers released during membrane trafficking events such as secretory, endocytic, autophagic, and phagocytic pathways. The membrane-enclosed area of the lysosome, called the lumen, contains hydrolytic enzymes active in an acidic environment. These acid hydrolases are functional at a pH between 4.5 and 5 and are involved in cellular processes such as cell signaling, energy metabolism, restoration of the plasma membrane,...
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...
Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...
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...

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Related Experiment Video

Updated: Jun 24, 2026

Interactions with and Membrane Permeabilization of Brain Mitochondria by Amyloid Fibrils
15:04

Interactions with and Membrane Permeabilization of Brain Mitochondria by Amyloid Fibrils

Published on: September 28, 2019

[Amyloidoses in neuropathology].

S Prokop1, W Stenzel, H H Goebel

  • 1Institut für Neuropathologie, Charité-Universitätsmedizin Berlin, Charitéplatz 1, 10117, Berlin, Deutschland.

Der Pathologe
|April 3, 2009
PubMed
Summary
This summary is machine-generated.

Amyloidosis is crucial in neuropathology, involving beta-amyloid deposition in the brain, often seen in older adults. Accurate diagnosis requires detailed amyloid characterization, especially in rare familial or prion diseases.

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Modeling Charcot-Marie-Tooth Disease In Vitro by Transfecting Mouse Primary Motoneurons

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Last Updated: Jun 24, 2026

Interactions with and Membrane Permeabilization of Brain Mitochondria by Amyloid Fibrils
15:04

Interactions with and Membrane Permeabilization of Brain Mitochondria by Amyloid Fibrils

Published on: September 28, 2019

A Caenorhabditis elegans Model System for Amylopathy Study
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A Caenorhabditis elegans Model System for Amylopathy Study

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Area of Science:

  • Neuropathology
  • Molecular Biology
  • Genetics

Context:

  • Amyloid deposition is a key feature in various neuropathologies, impacting both autopsy and biopsy analyses.
  • Cerebral amyloidoses, primarily involving beta-amyloid, predominantly affect individuals over 60.
  • Cerebral amyloid angiopathy (CAA) presents with intracerebral hemorrhage, while Alzheimer's disease manifests as dementia.

Purpose:

  • To highlight the significance of amyloidoses in neuropathology.
  • To differentiate clinical presentations of cerebral amyloidoses, including CAA and Alzheimer's disease.
  • To emphasize the necessity of thorough neuropathological assessment for rare amyloidosis forms and prion diseases.

Summary:

  • Amyloidosis is integral to neuropathology, characterized by beta-amyloid deposition, particularly in cerebral tissues of older patients.
  • Clinical manifestations vary, with CAA causing hemorrhage and Alzheimer's disease leading to dementia.
  • Rare familial amyloidoses and prion diseases necessitate detailed neuropathological evaluation and amyloid characterization.

Impact:

  • Improves understanding of amyloid-related neuropathologies.
  • Aids in accurate diagnosis and differentiation of neurological disorders.
  • Underscores the importance of comprehensive amyloid analysis in clinical practice and research.