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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...
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...
Diabetic Neuropathy01:22

Diabetic Neuropathy

DefinitionDiabetic neuropathy is nerve damage caused by long-standing diabetes mellitus. It results directly from prolonged high blood sugar levels.PathophysiologyThe pathophysiology of diabetic neuropathy involves both metabolic and vascular disturbances triggered by chronic hyperglycemia.Metabolic injury: Elevated glucose levels activate the polyol pathway within nerve cells, leading to the accumulation of sorbitol and fructose. This increases oxidative stress, disrupts normal nerve...
Myasthenia Gravis ll: Pathophysiology01:22

Myasthenia Gravis ll: Pathophysiology

The disease process of myasthenia gravis begins at the neuromuscular junction, where antibodies attack key proteins needed for muscle activation. This immune reaction weakens signal transmission, leading to the characteristic muscle fatigue and weakness that define the condition.Immune-Mediated DamageIn most individuals, antibodies target acetylcholine receptors (AChRs) on the postsynaptic membrane of muscle cells. By blocking acetylcholine binding, these antibodies prevent the nerve signal...
Alzheimer's Disease: Overview01:26

Alzheimer's Disease: Overview

Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ and tau...

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Related Experiment Video

Updated: May 16, 2026

Rapid Generation of Amyloid from Native Proteins In vitro
05:48

Rapid Generation of Amyloid from Native Proteins In vitro

Published on: December 5, 2013

Amyloid neuropathies.

Susan C Shin1, Jessica Robinson-Papp

  • 1Mount Sinai School of Medicine, New York, NY, USA.

The Mount Sinai Journal of Medicine, New York
|December 15, 2012
PubMed
Summary
This summary is machine-generated.

Systemic amyloidoses commonly cause peripheral neuropathy due to amyloid buildup in nerves. This review covers clinical presentations, diagnosis, and treatment of these complex neurological complications.

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Interactions with and Membrane Permeabilization of Brain Mitochondria by Amyloid Fibrils
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Interactions with and Membrane Permeabilization of Brain Mitochondria by Amyloid Fibrils

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Visualization of Amyloid β Deposits in the Human Brain with Matrix-assisted Laser Desorption/Ionization Imaging Mass Spectrometry
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Last Updated: May 16, 2026

Rapid Generation of Amyloid from Native Proteins In vitro
05:48

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Published on: December 5, 2013

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

Interactions with and Membrane Permeabilization of Brain Mitochondria by Amyloid Fibrils

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Visualization of Amyloid β Deposits in the Human Brain with Matrix-assisted Laser Desorption/Ionization Imaging Mass Spectrometry
09:31

Visualization of Amyloid β Deposits in the Human Brain with Matrix-assisted Laser Desorption/Ionization Imaging Mass Spectrometry

Published on: March 7, 2019

Area of Science:

  • Neurology
  • Genetics
  • Pathology

Background:

  • Peripheral neuropathy is a frequent complication of systemic amyloidoses.
  • Amyloid deposition in nerves is the likely cause of neuropathy.
  • Neuropathy can manifest as focal, multifocal, or diffuse nerve involvement.

Purpose of the Study:

  • To review inherited and acquired amyloidoses affecting the peripheral nervous system.
  • To detail the clinical presentation and neurological aspects of these diseases.
  • To emphasize diagnostic evaluation, treatment, and prognosis.

Main Methods:

  • Review of literature on systemic amyloidoses and peripheral neuropathy.
  • Emphasis on clinical presentation, physical examination findings.
  • Discussion of diagnostic evaluation, treatment, and prognosis.

Main Results:

  • Common phenotypes include sensorimotor polyneuropathy and carpal tunnel syndrome.
  • Autonomic neuropathy can affect multiple organ systems with non-specific symptoms.
  • Various types of amyloidosis, including familial, primary, secondary, and senile, are discussed.

Conclusions:

  • Peripheral neuropathy is a significant neurological manifestation of systemic amyloidoses.
  • Accurate diagnosis and management are crucial for improving patient outcomes.
  • Understanding the diverse clinical presentations is key to effective treatment.