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Related Concept Videos

Aging01:26

Aging

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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.
Cellular Clock Theory
The cellular clock theory posits that the human lifespan is closely tied to the finite capacity of cells to divide, a phenomenon governed by telomeres, which are protective caps at the ends of...
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The Effect of Aging on Tissues01:19

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Several body functions deteriorate with age. The external signs of aging are easily identifiable. For example, the skin becomes dry, less elastic, and thins out, forming wrinkles. The skin of the face begins to appear looser due to a decrease in the levels of elastic and collagen fibers in the connective tissue. Additionally, melanin production in the hair follicle decreases with age, resulting in gray hair. Moreover, the senses of sight and hearing decline, so glasses and hearing aids may...
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Replicative Cell Senescence02:15

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Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds...
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iPS Cell Differentiation01:22

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The ability of induced pluripotent stem cells or iPSCs to differentiate into most body cell types has stimulated repair and regenerative medicine research over the past few decades. iPSC-derived blood cells, hepatocytes, beta islet cells, cardiomyocytes, neurons, and other cell types can repair injuries or regenerate damaged tissue in diseases such as diabetes and neurodegenerative disorders.
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Parkinson's Disease: Overview01:15

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Neurodegenerative disorders are progressive diseases that cause irreversible damage and loss to neurons in specific brain areas. Examples of these disorders include Parkinson's disease, Alzheimer's disease, Multiple Sclerosis (MS), and Amyotrophic Lateral Sclerosis (ALS). These disorders share characteristics such as proteinopathies, selective neuronal vulnerability, and a complex interplay between genetic and environmental factors. The primary therapeutic goal for these conditions is...
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Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...
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Aging, Cellular Senescence, and Progressive Multiple Sclerosis.

Dimitrios Papadopoulos1, Roberta Magliozzi2, Dimos D Mitsikostas3

  • 1Molecular Carcinogenesis Group, Laboratory of Histology and Embryology, School of Health Sciences, National and Kapodistrian University of Athens, Athens, Greece.

Frontiers in Cellular Neuroscience
|July 23, 2020
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Summary
This summary is machine-generated.

Cellular senescence, a hallmark of aging, accelerates neurodegeneration in multiple sclerosis (MS). Targeting senescent cells may offer new neuroprotective therapies for MS progression.

Keywords:
cellular senescenceinflammationmultiple sclerosisneurodegenerationneuroprotectionremyelinationsenolytics

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Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • Aging is a primary risk factor for neurodegenerative diseases like multiple sclerosis (MS).
  • Cellular senescence (CS), a process linked to aging, involves cell-cycle arrest and a pro-inflammatory state.
  • Stressors in aging and MS pathology, including oxidative stress and mitochondrial dysfunction, trigger CS.

Purpose of the Study:

  • To explore the link between cellular senescence and the pathogenesis of multiple sclerosis.
  • To discuss the potential of senolytic and senomorphic agents in treating MS.

Main Methods:

  • Review of existing literature on cellular senescence, aging, and multiple sclerosis.
  • Analysis of the mechanisms by which senescent cells contribute to MS pathology.

Main Results:

  • Senescent cells accumulate with age and promote inflammation through secreted factors.
  • Accelerated CS in MS may drive disease progression by exacerbating inflammation, impairing neuronal function, and hindering remyelination.
  • Senescent cells contribute to blood-brain barrier dysfunction and neurodegeneration.

Conclusions:

  • Cellular senescence is implicated in the pathogenesis and progression of multiple sclerosis.
  • Senolytic and senomorphic therapies show promise as neuroprotective strategies for MS.