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Related Concept Videos

Neurons: The Axon01:21

Neurons: The Axon

Axons are long, cytoplasmic processes of nerve cells capable of propagating electrical impulses known as action potentials. The cytoplasm or axoplasm of an axon contains neurofibrils, neurotubules, small vesicles, lysosomes, mitochondria, and various enzymes, all encased within the axolemma, the plasma membrane of the axon.
The axon attaches to the cell body at a cone-shaped elevation called the axon hillock. The initial part of the axon, closest to the hillock, is known as the initial segment.
Overview of Cell Death01:30

Overview of Cell Death

Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the 20th century...
Neurogenesis and Regeneration of Nervous Tissue01:15

Neurogenesis and Regeneration of Nervous Tissue

In the CNS, neurogenesis, the birth of new neurons from stem cells, is limited to the hippocampus in adults. In other regions of the brain and spinal cord, neurogenesis is almost non-existent due to inhibitory influences from neuroglia, especially oligodendrocytes, and the absence of growth-stimulating cues. The myelin produced by oligodendrocytes in the CNS inhibits neuronal regeneration. Furthermore, astrocytes proliferate rapidly after neuronal damage, forming scar tissue that physically...
Necrosis01:16

Necrosis

Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become anucleated and die, but their...
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
Export of Misfolded Proteins out of the ER01:32

Export of Misfolded Proteins out of the ER

After folding, the ER assesses the quality of secretory and membrane proteins. The correctly folded proteins are cleared by the calnexin cycle for transport to their final destination, while misfolded proteins are held back in the ER lumen. The ER chaperones attempt to unfold and refold the misfolded proteins but sometimes fail to achieve the correct native conformation. Such terminally misfolded proteins are then exported to the cytosol by ER-associated degradation or ERAD pathway for...

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Related Experiment Video

Updated: Jun 13, 2026

Expanding the Toolkit for In Vivo Imaging of Axonal Transport
09:24

Expanding the Toolkit for In Vivo Imaging of Axonal Transport

Published on: December 23, 2021

Retrograde axonal transport: pathways to cell death?

Eran Perlson1, Sandra Maday, Meng-Meng Fu

  • 1Department of Physiology, University of Pennsylvania School of Medicine, Philadelphia, PA 19067, USA.

Trends in Neurosciences
|May 4, 2010
PubMed
Summary

Axonal transport is vital for neuron health, supplying essential components and clearing waste. Disruptions in this transport system are linked to neurodegenerative diseases like Alzheimer's and Parkinson's.

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Morphological and Functional Evaluation of Axons and their Synapses during Axon Death in Drosophila melanogaster

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An Ex Vivo Laser-induced Spinal Cord Injury Model to Assess Mechanisms of Axonal Degeneration in Real-time
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An Ex Vivo Laser-induced Spinal Cord Injury Model to Assess Mechanisms of Axonal Degeneration in Real-time

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Related Experiment Videos

Last Updated: Jun 13, 2026

Expanding the Toolkit for In Vivo Imaging of Axonal Transport
09:24

Expanding the Toolkit for In Vivo Imaging of Axonal Transport

Published on: December 23, 2021

Morphological and Functional Evaluation of Axons and their Synapses during Axon Death in Drosophila melanogaster
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Morphological and Functional Evaluation of Axons and their Synapses during Axon Death in Drosophila melanogaster

Published on: March 16, 2020

An Ex Vivo Laser-induced Spinal Cord Injury Model to Assess Mechanisms of Axonal Degeneration in Real-time
11:18

An Ex Vivo Laser-induced Spinal Cord Injury Model to Assess Mechanisms of Axonal Degeneration in Real-time

Published on: November 25, 2014

Area of Science:

  • Neuroscience
  • Cell Biology
  • Neurodegenerative Diseases

Background:

  • Active axonal transport is essential for neuronal function, supplying the synapse and clearing cellular waste.
  • Microtubule motors facilitate long-distance transport of proteins, lipids, and signaling endosomes.
  • While neurotrophic factor signaling is understood, stress-induced axonal signaling is an emerging area of research.

Purpose of the Study:

  • To explore the link between alterations in axonal transport and neurodegeneration.
  • To review evidence of transport defects in various neurodegenerative disease models.
  • To discuss the role of retrograde signaling in neuronal cell death.

Main Methods:

  • Review of existing literature on axonal transport and neurodegenerative diseases.
  • Analysis of evidence from models of amyotrophic lateral sclerosis, Huntington's, Parkinson's, and Alzheimer's disease.
  • Examination of the functional consequences of transport defects.

Main Results:

  • Defective transport of vesicles, mitochondria, degradative organelles, and signaling endosomes is observed in neurodegenerative disease models.
  • Axonal transport defects are sufficient to cause neurodegeneration.
  • Alterations in retrograde signaling pathways correlate with rapid neuronal cell death.

Conclusions:

  • Axonal transport is a critical factor in maintaining neuronal health.
  • Dysfunctional axonal transport is a significant contributor to neurodegeneration.
  • Retrograde signaling defects may drive rapid neuronal cell death in neurodegenerative conditions.