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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...
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: Jun 15, 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

Renal amyloidosis.

Helen J Lachmann1, Julian D Gillmore

  • 1National Amyloidosis Centre, UCL Medical School, Royal Free Hospital Campus, London.

British Journal of Hospital Medicine (London, England : 2005)
|March 12, 2010
PubMed
Summary
This summary is machine-generated.

Renal amyloidosis commonly causes kidney problems like proteinuria and impairment. While treatment can stabilize or improve kidney function, many patients still develop end-stage renal failure.

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Genetic Analysis of Hereditary Transthyretin Ala97Ser Related Amyloidosis
06:33

Genetic Analysis of Hereditary Transthyretin Ala97Ser Related Amyloidosis

Published on: June 9, 2018

Related Experiment Videos

Last Updated: Jun 15, 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

Genetic Analysis of Hereditary Transthyretin Ala97Ser Related Amyloidosis
06:33

Genetic Analysis of Hereditary Transthyretin Ala97Ser Related Amyloidosis

Published on: June 9, 2018

Area of Science:

  • Nephrology
  • Internal Medicine
  • Pathology

Background:

  • Systemic amyloidosis frequently leads to amyloid deposition in the kidneys.
  • Clinical presentation typically involves proteinuria and renal impairment.

Purpose of the Study:

  • To summarize the clinical implications of renal amyloid deposition in systemic amyloidosis.
  • To discuss the prognosis and management of kidney involvement.

Main Methods:

  • Review of existing literature on renal amyloidosis.
  • Analysis of clinical presentations and outcomes.

Main Results:

  • Renal involvement is a common manifestation of systemic amyloidosis.
  • Proteinuria and renal impairment are hallmark signs.
  • Effective treatment can lead to stabilization or improvement of renal function.
  • Despite treatment, a significant proportion of patients progress to end-stage renal failure.

Conclusions:

  • Renal amyloidosis significantly impacts patient outcomes in systemic amyloidosis.
  • Proactive management of the underlying condition and supportive renal care are crucial.
  • Further research may be needed to improve long-term renal survival rates.