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Related Concept Videos

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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,...
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Alzheimer's Disease: Overview01:26

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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.
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Aging01:26

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Aging is a complex biological phenomenon influenced by various processes that affect cellular and systemic functions. Several prominent theories attempt to explain its mechanisms, highlighting cellular limitations, oxidative damage, and hormonal changes as central factors in aging.
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Alzheimer's Disease (AD), a neurodegenerative disorder, is pathologically identified by amyloid plaques and neurofibrillary tangles composed of tau protein. AD pharmacotherapy aims to manage cognitive symptoms, delay disease progression, and treat behavioral symptoms. The treatment is primarily symptomatic and palliative, with no definitive disease-modifying therapy available. Cholinesterase inhibitors, including donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne), are...
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Related Experiment Video

Updated: Sep 29, 2025

Imaging the Intracellular Trafficking of APP with Photoactivatable GFP
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Imaging the Intracellular Trafficking of APP with Photoactivatable GFP

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Aging impact on amyloid precursor protein neuronal trafficking.

Tatiana Burrinha1, Cláudia Guimas Almeida1

  • 1Chronic Diseases Research Center (CEDOC), NOVA Medical School (NMS), Universidade Nova de Lisboa, 1169-056 Lisboa, Portugal.

Current Opinion in Neurobiology
|March 18, 2022
PubMed
Summary

Neuronal aging impacts membrane trafficking, potentially increasing Alzheimer

Area of Science:

  • Neuroscience
  • Cell Biology
  • Aging Research

Background:

  • Neuronal aging is linked to increased Alzheimer's disease risk.
  • Intraneuronal beta-amyloid (Aβ) accumulates in aged brains, independent of genetic mutations.
  • The role of neuronal aging in potentiating Aβ accumulation requires investigation.

Purpose of the Study:

  • To review how neuronal membrane trafficking maintains synapse function during aging.
  • To explore the link between aging, amyloid precursor protein (APP) trafficking, and Aβ production.
  • To identify molecular regulators of APP trafficking in aging neurons.

Main Methods:

  • Literature review focusing on neuronal membrane trafficking.
  • Analysis of APP processing and Aβ production in the context of aging.

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  • Examination of evidence linking aging to changes in membrane trafficking and APP metabolism.
  • Main Results:

    • Neuronal aging affects membrane trafficking dynamics.
    • Changes in membrane trafficking during aging influence APP processing.
    • Aging-related alterations in trafficking contribute to increased Aβ production.

    Conclusions:

    • Neuronal membrane trafficking is crucial for synapse function during aging.
    • Disruptions in APP trafficking during neuronal aging may drive Aβ accumulation.
    • Understanding these molecular mechanisms is key to developing strategies against synaptic decline and Alzheimer's disease.