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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.
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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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Metabolic States of the Body: Fasting and Starvation01:24

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During the initial hours of fasting, the body uses up its glycogen stores as an energy source. Once these glycogen reserves are depleted, the body begins breaking down stored triglycerides and structural proteins. During this stage, glycerol becomes a key substrate for gluconeogenesis, while free fatty acids undergo beta-oxidation to provide energy for tissues, such as skeletal muscle. In the fasting state, the body spares protein breakdown as much as possible to conserve muscle and structural...
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Metabolic States of the Body: The Postabsorptive State01:18

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The postabsorptive state usually starts about four hours after a meal and lasts until the next meal is eaten. During this time, the digestive system stops absorbing nutrients, and the body uses stored energy reserves to maintain stable blood glucose levels.
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Neurogenesis and Regeneration of Nervous Tissue01:15

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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...
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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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Related Experiment Video

Updated: Apr 26, 2026

Quantification of Subcellular Glycogen Distribution in Skeletal Muscle Fibers using Transmission Electron Microscopy
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Neuronal glycogen synthesis contributes to physiological aging.

Christopher Sinadinos1, Jordi Valles-Ortega, Laura Boulan

  • 1Institute for Research in Biomedicine (IRB Barcelona), Barcelona, Spain.

Aging Cell
|July 26, 2014
PubMed
Summary
This summary is machine-generated.

Neuronal glycogen accumulation contributes to brain aging and neurological decline. Reducing glycogen synthesis in mice and flies improved neurological function and extended lifespan, suggesting a key role in aging.

Keywords:
Drosophilaagingcorpora amylaceaglycogenprotein aggregationstress response

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Biochemistry

Background:

  • Glycogen, the primary carbohydrate energy store in animals, is found in brain glial cells and neurons.
  • Mutations affecting glycogen synthesis proteins cause Lafora bodies (LBs), leading to neurodegeneration in Lafora's disease.
  • Corpora amylacea (CA), similar to LBs, accumulate in aged human neurons, but their formation and consequences are unknown.

Purpose of the Study:

  • To investigate the role of neuronal glycogen accumulation in brain aging.
  • To explore the mechanisms and functional consequences of glycogen aggregate formation in aging neurons.
  • To determine if reducing glycogen synthesis impacts age-related neurological decline.

Main Methods:

  • Examined aged wild-type mice for glycogen-based aggregates in the brain.
  • Utilized genetic ablation of glycogen synthase in mice and Drosophila to assess its impact on aggregate formation.
  • Investigated the effects of reducing glycogen synthase in Drosophila neurons on neurological function and lifespan.

Main Results:

  • Aged mice accumulate glycogen-based aggregates in the brain, immunopositive for metabolic and stress-response proteins.
  • Genetic ablation of glycogen synthase prevented aggregate formation in aged mouse and fly brains.
  • Reducing glycogen synthase in Drosophila neurons improved age-related neurological function and extended lifespan.

Conclusions:

  • Neuronal glycogen accumulation contributes to physiological brain aging.
  • Glycogen aggregate formation is a key factor in age-related neurological decline.
  • Targeting glycogen synthesis may offer therapeutic strategies for age-related neurological disorders.