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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 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 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...
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Parkinson Disease ll: Pathophysiology01:24

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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: May 10, 2026

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

Hereditary and sporadic beta-amyloidoses.

Giuseppe Di Fede1, Giorgio Giaccone, Fabrizio Tagliavini

  • 1Division of Neurology 5-Neuropathology, IRCCS Foundation, Carlo Besta Neurological Institute, Milan, Italy. gdifede@istituto-besta.it

Frontiers in Bioscience (Landmark Edition)
|June 11, 2013
PubMed
Summary

Cerebral amyloidoses, like Alzheimer's disease and cerebral amyloid angiopathy, involve misfolded protein deposits in the brain. This review differentiates their pathways, clinical signs, and neuropathology for better diagnosis.

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Last Updated: May 10, 2026

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

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Published on: March 7, 2019

Genetic Analysis of Hereditary Transthyretin Ala97Ser Related Amyloidosis
06:33

Genetic Analysis of Hereditary Transthyretin Ala97Ser Related Amyloidosis

Published on: June 9, 2018

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

Area of Science:

  • Neurodegenerative diseases
  • Neuropathology
  • Protein misfolding disorders

Background:

  • Cerebral amyloidoses are progressive neurodegenerative conditions.
  • Caused by aggregated misfolded proteins in the central nervous system.
  • Lead to cognitive deficits, stroke, and neurological dysfunction.

Purpose of the Study:

  • Review differences in parenchymal and cerebrovascular beta-amyloidosis pathways.
  • Describe clinical, neuropathological, and biochemical characteristics.
  • Distinguish between familial and sporadic beta-amyloidosis phenotypes.

Main Methods:

  • Literature review of cerebral amyloidoses.
  • Analysis of beta-amyloid deposition pathways.
  • Comparison of clinico-pathological entities.

Main Results:

  • Beta-amyloidoses include Alzheimer's disease and cerebral amyloid angiopathy.
  • These conditions differ in protein deposition sites (parenchymal vs. vascular).
  • Familial and sporadic forms exhibit distinct phenotypes.

Conclusions:

  • Understanding pathway differences aids in distinguishing beta-amyloidosis forms.
  • Clinical and neuropathological features are key for diagnosis.
  • Further research into specific phenotypes can improve patient management.