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Related Concept Videos

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...
Neural Regulation01:37

Neural Regulation

Digestion begins with a cephalic phase that prepares the digestive system to receive food. When our brain processes visual or olfactory information about food, it triggers impulses in the cranial nerves innervating the salivary glands and stomach to prepare for food.
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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Dementia is an acquired, progressive syndrome characterized by a decline in multiple cognitive domains severe enough to impair daily functioning and reduce independence. Although memory loss is a central feature, the diagnosis requires additional deficits involving language, executive function, visuospatial skills, judgment, calculation, or abstract reasoning. These cognitive impairments reflect underlying neurodegenerative or vascular processes that gradually disrupt neuronal networks...

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Related Experiment Video

Updated: May 12, 2026

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

Defective regulated secretion: A trigger for Alzheimer's pathology?

Bhavna Verma1, Preman Singh2, Deborah C I Goberdhan3

  • 1Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford, UK.

Progress in Neurobiology
|May 10, 2026
PubMed
Summary
This summary is machine-generated.

Alzheimer's Disease (AD) neurodegeneration may stem from intraneuronal endolysosome defects, potentially triggered by Amyloid-β (Aβ) accumulation during regulated secretion. Targeting these early intracellular pathways offers novel therapeutic strategies for AD.

Keywords:
amyloid plaquesdense-core granules (DCGs)exosomesmultivesicular bodies (MVBs)neurofibrillary tanglestau– Amyloid-β (Aβ)

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Pathology

Background:

  • Alzheimer's Disease (AD) is characterized by amyloid plaques and neurofibrillary tangles.
  • Intraneuronal endolysosome defects are increasingly implicated as an early trigger for AD neurodegeneration.
  • These defects may be induced by Amyloid-β (Aβ) and tau pathologies.

Purpose of the Study:

  • To investigate the role of regulated secretion in initiating intraneuronal endolysosome defects in AD.
  • To explore novel intracellular mechanisms driving neurodegeneration in early AD.
  • To identify potential therapeutic targets for early AD intervention.

Main Methods:

  • Analysis of intracellular trafficking in neuronal and non-neuronal cells using high-resolution techniques.
  • Investigating the interplay between Amyloid Precursor Protein (APP), secretases, and endolysosomal compartments.
  • Examining the impact of Aβ accumulation and C-terminal fragments on endolysosomal function.

Main Results:

  • Aberrant compartmental maturation during regulated secretion leads to endolysosome defects.
  • APP, secretases, and endosomal compartments converge during these aberrant events.
  • Aβ accumulation interferes with endolysosomal trafficking and may induce tau pathology.
  • Secreted proteins from Aβ-laden compartments can induce endolysosomal phenotypes in other cells.

Conclusions:

  • Regulated secretion plays a critical role in the initiation of AD pathology via intraneuronal endolysosome dysfunction.
  • Novel intracellular pathways driving neurodegeneration are highlighted.
  • Identifying suppressors of these pathways could lead to new early-stage AD therapies.