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Related Concept Videos

Aging01:26

Aging

1.1K
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

The Effect of Aging on Tissues

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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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Pharmacodynamics in Geriatric Patients: Effects of Age01:27

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Age-related pharmacokinetic changes are extensively documented, but understanding age-related pharmacodynamic alterations is relatively limited. This knowledge gap can be partly attributed to the complexity of developing appropriate measures of drug responses compared to bioanalytical methods for determining drug concentrations.Most information regarding age-related differences in human pharmacodynamics originates from cross-sectional studies. However, these studies assume that observed mean...
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Alzheimer Disease l: Introduction01:29

Alzheimer Disease l: Introduction

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Alzheimer disease is a chronic, progressive, and irreversible neurodegenerative disorder and the most common cause of dementia in older adults. It leads to gradual neuronal loss, causing cognitive decline, behavioral changes, and loss of functional independence.Risk Factors and EtiologyThe disease is multifactorial. Age is the strongest risk factor, with prevalence doubling every 5 years after age 65. Genetic factors include mutations in genes such as APP, PSEN1, and PSEN2, which are associated...
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Alzheimer Disease ll: Pathophysiology01:23

Alzheimer Disease ll: Pathophysiology

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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...
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Bone Disorders01:29

Bone Disorders

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Aging and its effect on bone remodeling is the most common cause of bone disorders. In young and healthy people, bone deposition and resorption happen at an equal rate to maintain optimal bone health.
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Related Experiment Video

Updated: May 4, 2026

Use of Synaptic Zinc Histochemistry to Reveal Different Regions and Laminae in the Developing and Adult Brain
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Use of Synaptic Zinc Histochemistry to Reveal Different Regions and Laminae in the Developing and Adult Brain

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Zinc and the aging brain.

Johnathan R Nuttall1, Patricia I Oteiza

  • 1Department of Nutrition, University of California, One Shields Av., Davis, CA, 95616, USA.

Genes & Nutrition
|December 25, 2013
PubMed
Summary

Altered zinc homeostasis is linked to Alzheimer's disease (AD) and dementia. Restoring zinc balance may offer therapeutic benefits for AD and improve glycemic control in the elderly.

Area of Science:

  • Neuroscience
  • Biochemistry
  • Gerontology

Background:

  • Trace element homeostasis, particularly zinc, is crucial for physiological functions.
  • Aging affects zinc homeostasis, with observed alterations in zinc distribution in Alzheimer's disease (AD).
  • The precise role of zinc and other metals in AD pathology is still under investigation.

Purpose of the Study:

  • To review current knowledge on the pathological and protective roles of brain zinc in Alzheimer's disease.
  • To identify potential therapeutic strategies targeting zinc homeostasis for AD treatment.
  • To explore the impact of zinc supplementation on AD and diabetes mellitus in the elderly.

Main Methods:

  • Literature review of studies on zinc, trace elements, and neurodegenerative diseases.

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  • Analysis of research on cellular and systemic zinc distribution in aging and AD.
  • Examination of clinical trial data for zinc supplementation in AD and diabetes.

    • Main Results:

    • Evidence suggests altered zinc homeostasis in AD, potentially contributing to disease pathology.
    • Zinc supplementation shows promise for benefiting individuals with AD and improving glycemic control in elderly diabetics.
    • Genetic polymorphisms may influence individual zinc requirements for supplementation.

    Conclusions:

    • Restoring zinc homeostasis represents a potential therapeutic avenue for Alzheimer's disease.
    • Further research is needed to elucidate the mechanisms of zinc in AD and optimize supplementation strategies.
    • Considering genetic factors is important for personalized zinc supplementation plans.