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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...
Alzheimer Disease l: Introduction01:29

Alzheimer Disease l: Introduction

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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Atypical pneumonia, often caused by Mycoplasma pneumoniae, is a form of pulmonary infection that differs from the classical presentation of bacterial pneumonia in both its cause and clinical symptoms. Mycoplasma pneumoniae is a pleomorphic bacterium notable for its lack of a rigid cell wall. This structural characteristic imparts resistance to beta-lactam antibiotics and significantly influences the bacterium’s behavior within the human host.Other pathogens responsible for the disease include...
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Emphysema, a major phenotype of chronic obstructive pulmonary disease (COPD), is characterized by irreversible destruction of alveolar walls and permanent enlargement of distal airspaces. Unlike chronic bronchitis, which primarily affects the airways, emphysema predominantly involves the lung parenchyma, where structural damage leads to airflow limitation.PathophysiologyIt most commonly results from prolonged exposure to cigarette smoke and other toxic gases, particularly cigarette smoke.

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Updated: Jun 13, 2026

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

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Published on: December 5, 2013

Primary amyloidosis causing diffuse alveolar hemorrhage.

Max Shenin1, Wen Xiong, Manisha Naik

  • 1Division of Rheumatology, Thomas Jefferson University, Philadelphia, PA 19107, USA.

Journal of Clinical Rheumatology : Practical Reports on Rheumatic & Musculoskeletal Diseases
|April 24, 2010
PubMed
Summary

Vascular amyloidosis can mimic vasculitis, causing diffuse alveolar hemorrhage. Early diagnosis is crucial to avoid misdiagnosis and inappropriate treatments, improving patient outcomes.

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Area of Science:

  • Pulmonary Medicine
  • Nephrology
  • Rheumatology

Background:

  • Diffuse alveolar hemorrhage (DAH) is a severe pulmonary complication.
  • It is associated with vasculitic syndromes and conditions mimicking vasculitis.
  • Distinguishing DAH causes is critical for effective management.

Observation:

  • A 79-year-old male presented with cough, bloody sputum, and respiratory failure.
  • Initial tests showed atypical antineutrophil cytoplasmic antibodies.
  • Lung biopsy revealed amyloid deposition in blood vessels.

Findings:

  • The patient was diagnosed with vascular amyloidosis presenting as DAH.
  • Treatment with intravenous methylprednisolone led to rapid improvement.
  • This case highlights unusual presentations of vascular amyloidosis.

Implications:

  • Vascular amyloidosis can present with clinical features similar to vasculitis.
  • Accurate diagnosis is essential to prevent harmful treatments.
  • Timely diagnosis can improve patient prognosis and treatment efficacy.