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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 microglia. Abnormal...
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Alzheimer's disease: an evolutionary approach.

Enric Bufill1, Rafael Blesa2, Jordi Augustí3

  • 1Departement of Neurology, Vic Hospital Consortium, Francesc Plá 1, E-08500, Vic, Spain; Institute of Human Paleoecology and Social Evolution, Rovira i Virgili University, Tarragona, Spain, ebufill@telefonica.net.

Journal of Anthropological Sciences = Rivista Di Antropologia : JASS
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Summary

Alzheimer's disease (AD) is uniquely common in humans due to evolutionary brain changes, making specific neurons vulnerable. These changes, linked to synaptic plasticity and oxidative stress, may explain human susceptibility to AD.

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Area of Science:

  • Neuroscience
  • Evolutionary Biology
  • Genetics

Background:

  • Alzheimer's disease (AD) is a prevalent, age-related neurodegenerative disorder with incompletely understood causes.
  • AD's high incidence in humans versus its rarity in other mammals suggests an evolutionary basis for human vulnerability.

Purpose of the Study:

  • To explore the evolutionary perspective of Alzheimer's disease (AD) to understand the root causes of human susceptibility.
  • To investigate how evolutionary changes in the human brain may have conferred vulnerability to AD.

Main Methods:

  • Comparative analysis of AD prevalence across species.
  • Examination of genetic factors, synaptic plasticity, and oxidative stress in neuronal function.
  • Review of neurodevelopmental and metabolic characteristics of human neurons.

Main Results:

  • Human-specific evolutionary alterations in the brain, particularly in neurons retaining juvenile characteristics, increase vulnerability to AD triggers.
  • Genes associated with AD are often linked to synaptic plasticity, and oxidative stress plays a significant role.
  • These neuronal changes, potentially driven by adaptations for cognitive functions, may represent a trade-off (antagonistic pleiotropy) increasing AD risk.

Conclusions:

  • An evolutionary approach integrating data from various disciplines offers a novel framework for understanding complex diseases like Alzheimer's.
  • Human brain evolution, while enabling advanced cognition, may have inadvertently created a biological susceptibility to AD.
  • Understanding these evolutionary legacies is crucial for developing new strategies to combat Alzheimer's disease.