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Related Concept Videos

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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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
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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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Atherosclerosis is a progressive disorder characterized by the buildup of plaques on the arterial inner wall, causing them to narrow and harden over time. These plaques comprise lipids, calcium, blood components, carbohydrates, and fibrous tissue. The process primarily affects the intima of large and medium-sized arteries, reducing blood flow in any artery.Etiology and risk factorsThe cause of atherosclerosis is multifactorial, involving a complex interplay among endothelial injury, lipid...
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Detection of Nuclear Blebbing and DNA Leakage in Mammalian Cells by Immunofluorescence
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Lamin A to Z in normal aging.

Stanley R Primmer1, Chen-Yu Liao2, Oona M P Kummert2

  • 1Independent Affiliation, Lauderhill, FL 33319, USA.

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Prelamin A accumulation, a nuclear protein precursor, may drive normal aging processes. Understanding these mechanisms could lead to interventions extending healthspan and lifespan.

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Area of Science:

  • Cell biology
  • Molecular biology
  • Gerontology

Background:

  • Mutations in the LMNA gene cause Hutchinson-Gilford progeria syndrome (HPGS).
  • The common HPGS mutation produces progerin, a lamin A splice variant linked to accelerated aging.
  • Emerging evidence suggests prelamin A, a lamin A precursor, accumulates with normal aging and may drive age-related pathology.

Purpose of the Study:

  • To elucidate the mechanisms behind prelamin A accumulation during aging.
  • To present evidence supporting prelamin A's role as a driver of normative aging.
  • To identify potential therapeutic targets for age-related diseases.

Main Methods:

  • Analysis of prelamin A processing and accumulation in aging models.
  • Investigation of the functional consequences of prelamin A accumulation.
  • Comparative studies with progerin and its role in progeroid syndromes.

Main Results:

  • Prelamin A, not just progerin, accumulates with age and impacts cellular function.
  • Mechanisms driving prelamin A accumulation in aging are identified.
  • Prelamin A shares pathological properties with progerin, suggesting a common pathway.

Conclusions:

  • Prelamin A accumulation is a significant factor in normal aging.
  • Targeting prelamin A pathways offers a strategy to improve healthspan and lifespan.
  • Further research into prelamin A is crucial for developing anti-aging interventions.