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Alzheimer disease.

Ana Laura Calderon-Garcidueñas1, Charles Duyckaerts2

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Summary

Alzheimer disease involves amyloid-beta (Aβ) plaques and tau tangles, leading to brain atrophy and neuronal loss. While Aβ deposition may initiate the disease, tau pathology correlates more closely with Alzheimer

Keywords:
Alzheimer disease neuropathologyabeta depositneurofibrillary tangleneuronal lossneuropathological criteriasenile plaquesynaptic losstau aggregation

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Area of Science:

  • Neuropathology
  • Neurodegenerative Diseases
  • Alzheimer Disease Research

Background:

  • Alzheimer disease (AD) is defined by extracellular amyloid-beta (Aβ) peptide accumulation and intracellular hyperphosphorylated tau aggregation.
  • Disease progression involves macroscopic brain atrophy, particularly in the entorhinal area, hippocampus, amygdala, and neocortex, alongside locus coeruleus depigmentation.
  • Pathological hallmarks include diffuse Aβ deposits evolving into focal amyloid plaques with tau-positive neurites, and tau pathology spreading through specific brain regions.

Purpose of the Study:

  • To outline the characteristic neuropathological features of Alzheimer disease.
  • To describe the spatiotemporal progression of Aβ deposition (Thal phases) and tau pathology (Braak stages).
  • To highlight associated neurodegenerative processes such as synaptic loss, neuronal loss, granulovacuolar degeneration, and perisomatic granules.

Main Methods:

  • Histopathological examination of post-mortem brain tissue.
  • Immunohistochemical staining for Aβ and hyperphosphorylated tau.
  • Assessment of macroscopic brain atrophy and specific cellular changes.

Main Results:

  • Aβ deposition follows a predictable pattern, starting in the neocortex and progressing to the hippocampus, striatum, mesencephalon, and cerebellum.
  • Tau pathology also exhibits a stereotyped progression, beginning in the brainstem and entorhinal area, then spreading to the hippocampus and neocortex.
  • Synaptic loss, neuronal loss, granulovacuolar degeneration, and perisomatic granules are observed in conjunction with Aβ and tau pathology.

Conclusions:

  • The neuropathology of Alzheimer disease is characterized by the distinct and progressive deposition of Aβ and tau.
  • While familial cases suggest Aβ deposition as an early event, tau pathology appears to correlate more strongly with clinical symptoms.
  • The precise physiopathology of Alzheimer disease remains an area of active investigation.