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Related Concept Videos

Gene-Environment Interactions01:20

Gene-Environment Interactions

Gene expression is a dynamic process that is significantly influenced by environmental factors. This interaction underlies the complex nature of biological development and the phenotypic differences observed among individuals, even among those with identical genetic makeups. Factors such as radiation, temperature, behavior, nutrition, and stress play pivotal roles in determining how genes are expressed. The concept of the reaction range is central to understanding this interaction. It posits...
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Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
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Amyloid Fibrils03:03

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Epigenetic Regulation01:37

Epigenetic Regulation

Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
X-chromosome...
Epigenetic Regulation01:46

Epigenetic Regulation

Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
Epigenetic Regulation01:46

Epigenetic Regulation

Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.

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Quantitative 3D In Silico Modeling (q3DISM) of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease
09:33

Quantitative 3D In Silico Modeling (q3DISM) of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease

Published on: December 26, 2016

The environment, epigenetics and amyloidogenesis.

Jinfang Wu1, Md Riyaz Basha, Nasser H Zawia

  • 1Department of Biomedical and Pharmaceutical Sciences, University of Rhode Island, Kingston, RI 02881, USA.

Journal of Molecular Neuroscience : MN
|December 25, 2007
PubMed
Summary

Environmental exposure, such as lead (Pb), during development may increase Alzheimer's Disease (AD) risk later in life. Epigenetic changes, specifically DNA methylation, may mediate this link between early exposure and later AD pathogenesis.

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Area of Science:

  • Neuroscience
  • Toxicology
  • Epigenetics

Background:

  • Alzheimer's Disease (AD) is a progressive neurodegenerative disorder characterized by beta-amyloid (Abeta) plaques and hyperphosphorylated tau.
  • While genetic factors are known, over 90% of AD cases are sporadic, suggesting environmental influences are critical.
  • Developmental exposure to environmental toxins like lead (Pb) may contribute to AD pathogenesis later in life.

Purpose of the Study:

  • To investigate the role of epigenetics in mediating the link between early-life environmental exposure and the development of Alzheimer's Disease.
  • To explore how lead (Pb) exposure during development influences Abeta production and oxidative stress markers in aging brains.
  • To examine alterations in DNA methylation profiles in gene promoters as a mechanism for Pb-induced, age-dependent AD pathology.

Main Methods:

  • Utilizing rodent models developmentally exposed to lead (Pb).
  • Measuring amyloid precursor protein (APP) and Abeta levels in aging brains.
  • Assessing oxidative DNA damage markers like 8-oxo-dG.
  • Analyzing CpG methylation patterns in gene promoters to understand epigenetic modifications.

Main Results:

  • Developmental lead (Pb) exposure increased APP and Abeta production in aged rodents.
  • Lead (Pb) exposure led to elevated oxidative stress markers (8-oxo-dG) in older animals.
  • Lead (Pb) exposure promoted amyloidogenic histopathology in primate models.
  • Evidence suggests epigenetic pathways, particularly DNA methylation changes, underlie Pb-induced latent pathogenesis.

Conclusions:

  • Early-life environmental exposures, such as lead (Pb), can have long-lasting effects on brain health and AD risk.
  • Epigenetic mechanisms, specifically alterations in DNA methylation, are likely involved in mediating the connection between early environmental insults and late-onset neurodegeneration.
  • These findings highlight the importance of environmental factors and epigenetic modifications in Alzheimer's Disease etiology.