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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...
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 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...
Myasthenia Gravis: Overview and Treatment01:20

Myasthenia Gravis: Overview and Treatment

Myasthenia gravis is a neuromuscular transmission disorder characterized by weakness and increased fatigability of skeletal muscles. It is an autoimmune disease affecting approximately one in 2000 people, where antibodies against the α1 subunit of nicotinic acetylcholine receptors are produced.
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Chemical Synapses01:26

Chemical Synapses

Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
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Updated: Jun 24, 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

Autonomic failure in primary amyloidosis.

Aditi Pandit1, Savita Gangurde, S B Gupta

  • 1Medicine and Cardiology, Bharat Ratna Dr. Babasaheb Ambedkar Memorial Hospital, Central Railway, Byculla, Mumbai.

The Journal of the Association of Physicians of India
|March 28, 2009
PubMed
Summary

Primary Amyloidosis, a rare plasma cell disorder, typically affects multiple systems. This case highlights a unique presentation of pure autonomic failure without peripheral nerve involvement, challenging existing documentation.

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Last Updated: Jun 24, 2026

Rapid Generation of Amyloid from Native Proteins In vitro
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Published on: December 5, 2013

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

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Performing and Processing FNA of Anterior Fat Pad for Amyloid
09:41

Performing and Processing FNA of Anterior Fat Pad for Amyloid

Published on: October 30, 2010

Area of Science:

  • Neurology
  • Hematology
  • Pathology

Background:

  • Amyloidosis is a rare plasma cell dyscrasia characterized by extracellular amyloid protein deposition in tissues.
  • Primary Amyloidosis affects multiple systems, with peripheral nerve involvement occurring in 20% of cases.
  • Polyneuropathy is a common manifestation, but pure autonomic failure without nerve involvement is undocumented.

Observation:

  • A case of Primary Amyloidosis presented with symptoms solely of autonomic dysfunction.
  • The patient exhibited pure autonomic failure (dysautonomia).
  • Peripheral nerve examination did not reveal significant neuropathy.

Findings:

  • This case represents a novel presentation of Primary Amyloidosis.
  • Pure autonomic failure is identified as a potential, albeit rare, manifestation of Primary Amyloidosis.
  • The findings expand the clinical spectrum of this multisystem disorder.

Implications:

  • Clinicians should consider Primary Amyloidosis in cases of unexplained pure autonomic failure.
  • Further research is needed to understand the mechanisms underlying this presentation.
  • This case may prompt re-evaluation of diagnostic criteria and clinical suspicion for amyloidosis.