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Related Concept Videos

Autophagy01:27

Autophagy

Autophagy is a self-digesting process by which a cell protects itself from threats both within and outside the cell, ranging from abnormal proteins to invading bacteria. In this process, obsolete components of the cell and invading microbes are degraded by hydrolytic enzymes active in an acidic environment of the lysosomal lumen.
An autophagic pathway consists of a series of signaling events activated in response to diverse stress and physiological conditions such as food deprivation,...
Delivery Pathways to the Lysosome01:36

Delivery Pathways to the Lysosome

Eukaryotic cells use different mechanisms to eliminate toxic waste obsolete and worn-out substances. Lysosomes play a pivotal role in this, and hence, these substances are carried to the lysosome from other parts of the cell and extracellular space through different pathways. The most elaborately studied pathways to the lysosome are the endocytic pathways.
Endocytosis
In endocytosis, the cell membrane takes up macromolecules and particles from the surrounding medium. Clathrin-mediated...
Autophagic Cell Death01:18

Autophagic Cell Death

Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and pro-apoptotic...
Lysosomal Hydrolases01:22

Lysosomal Hydrolases

Lysosomes are the site for the degradation of macromolecules and biological polymers released during membrane trafficking events such as secretory, endocytic, autophagic, and phagocytic pathways. The membrane-enclosed area of the lysosome, called the lumen, contains hydrolytic enzymes active in an acidic environment. These acid hydrolases are functional at a pH between 4.5 and 5 and are involved in cellular processes such as cell signaling, energy metabolism, restoration of the plasma membrane,...
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...
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...

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Related Experiment Video

Updated: May 26, 2026

A Novel In Vitro Live-imaging Assay of Astrocyte-mediated Phagocytosis Using pH Indicator-conjugated Synaptosomes
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Autophagy in dementias.

Christine Lund Kragh1, Kiren Ubhi, Tony Wyss-Coray

  • 1Department of Biomedicine, University of Aarhus, Aarhus, Denmark.

Brain Pathology (Zurich, Switzerland)
|December 14, 2011
PubMed
Summary
This summary is machine-generated.

Dementia, including Alzheimer's disease, involves protein buildup due to impaired cellular clearance. This review highlights altered autophagy as a common factor across various dementia types, impacting daily function.

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Last Updated: May 26, 2026

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Area of Science:

  • Neuroscience
  • Cellular Biology
  • Pathology

Background:

  • Dementias encompass a range of neurocognitive disorders, including Alzheimer's disease (AD), dementia with Lewy bodies (DLB), frontotemporal dementia (FTD), vascular dementia (VaD), and HIV-associated neurocognitive disorders (HAND).
  • These conditions are characterized by cognitive and social impairments affecting daily functioning, often linked to abnormal protein accumulation in the brain.
  • Deficits in cellular protein clearance pathways, such as autophagy and the ubiquitin-proteasome system, are implicated in the pathogenesis of dementia.

Purpose of the Study:

  • To review recent literature on the role of protein clearance pathways in various dementia disorders.
  • To identify common themes in the pathogenesis of dementias, specifically focusing on alterations in autophagy.
  • To explore the connection between impaired autophagy and the progression of neurodegenerative diseases.

Main Methods:

  • Systematic review of recent scientific literature on dementia and cellular protein clearance mechanisms.
  • Analysis of studies investigating the autophagocytic pathway in different types of dementia.
  • Synthesis of findings related to protein accumulation and clearance deficits in neurodegeneration.

Main Results:

  • Abnormal accumulation of proteins is a shared feature across the spectrum of dementias.
  • Alterations in the levels and function of autophagy, a key cellular protein clearance pathway, are frequently reported in various dementias.
  • Deficits in protein degradation contribute to the neuropathology observed in neurocognitive disorders.

Conclusions:

  • Altered autophagy is a common underlying mechanism implicated in the pathogenesis of diverse dementia disorders.
  • Understanding the role of autophagy in protein clearance offers potential therapeutic targets for dementia treatment.
  • Further research into autophagy modulation may provide insights into preventing or slowing dementia progression.