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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...
Parkinson Disease ll: Pathophysiology01:24

Parkinson Disease ll: Pathophysiology

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: Jun 3, 2026

Imaging the Intracellular Trafficking of APP with Photoactivatable GFP
07:55

Imaging the Intracellular Trafficking of APP with Photoactivatable GFP

Published on: October 17, 2015

Amyloid precursor protein processing and Alzheimer's disease.

Richard J O'Brien1, Philip C Wong

  • 1Department of Neurology, Johns Hopkins Bayview Medical Center, USA. robrien@jhmi.edu

Annual Review of Neuroscience
|April 5, 2011
PubMed
Summary

Alzheimer's disease involves amyloid-beta peptide (Aβ) buildup due to amyloid precursor protein (APP) breakdown. Understanding APP metabolism is key to developing new Alzheimer's disease therapies.

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Last Updated: Jun 3, 2026

Imaging the Intracellular Trafficking of APP with Photoactivatable GFP
07:55

Imaging the Intracellular Trafficking of APP with Photoactivatable GFP

Published on: October 17, 2015

Purification and Aggregation of the Amyloid Precursor Protein Intracellular Domain
10:08

Purification and Aggregation of the Amyloid Precursor Protein Intracellular Domain

Published on: August 28, 2012

Fabrication of Amyloid-β-Secreting Alginate Microbeads for Use in Modelling Alzheimer's Disease
06:52

Fabrication of Amyloid-β-Secreting Alginate Microbeads for Use in Modelling Alzheimer's Disease

Published on: July 6, 2019

Area of Science:

  • Neuroscience
  • Biochemistry
  • Genetics

Background:

  • Alzheimer's disease (AD) is the primary cause of dementia globally.
  • AD pathology includes brain accumulation of beta-amyloid peptide (Aβ) and tau protein.
  • Aβ generation from amyloid precursor protein (APP) proteolysis is critical in AD development.

Purpose of the Study:

  • To investigate the role of amyloid precursor protein (APP) metabolism in Alzheimer's disease (AD).
  • To understand the mechanisms behind neurotoxic Aβ peptide accumulation in the brain.
  • To identify potential therapeutic targets for AD based on APP processing.

Main Methods:

  • Biochemical analysis of amyloid precursor protein (APP) processing.
  • Genetic studies examining APP metabolism and Aβ generation.
  • Behavioral research in models of Alzheimer's disease.

Main Results:

  • Physiologic generation of neurotoxic Aβ peptide from sequential APP proteolysis is a crucial step in AD.
  • APP is a single-pass transmembrane protein rapidly metabolized in the brain.
  • The γ-secretase complex plays a role in APP processing and Aβ generation.

Conclusions:

  • Understanding APP metabolism and Aβ elimination is essential for clarifying Aβ accumulation in AD.
  • Insights from APP processing studies are vital for developing therapeutic strategies against Alzheimer's disease.