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Basic Science and Pathogenesis.

Antonios Dougalis1, Polina Abushik1, Anssi Pelkonen1

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This study reveals how amyloid-beta (Aβ) and tau pathology in Alzheimer's disease (AD) alters neuronal function. Idiopathic normal pressure hydrocephalus (iNPH) biopsies show synaptic changes and hyperexcitability, offering insights into early AD progression.

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Area of Science:

  • Neuroscience
  • Neuropathology
  • Human tissue research

Background:

  • Alzheimer's disease (AD) mechanisms are poorly understood due to limited early-stage human brain tissue.
  • Idiopathic normal pressure hydrocephalus (iNPH) offers a unique model, as some patients exhibit early AD pathology.
  • Surgically excised iNPH brain biopsies provide a novel human-based preclinical resource for AD research.

Purpose of the Study:

  • To investigate the impact of early Alzheimer's disease (AD) related pathology on human neuronal function.
  • To establish and utilize idiopathic normal pressure hydrocephalus (iNPH) brain biopsies as a preclinical model for AD.
  • To correlate cellular and network-level electrophysiological changes with AD-related pathological markers.

Main Methods:

  • Developed a pipeline to analyze neuronal properties in iNPH biopsies using patch clamp and multi-electrode array (MEA).
  • Performed integrative analysis of human neuronal electrophysiology and cellular morphology.
  • Correlated electrophysiological findings with existing AD-related pathologies (Aβ and tau).

Main Results:

  • Amyloid-beta (Aβ) deposits decreased L1-induced inhibition and caused hyperexcitability.
  • Increased global spine density was observed in pyramidal neurons with AD pathology.
  • Neurons with both Aβ and tau showed intrinsic property deficits and increased bursting under NMDA stimulation.

Conclusions:

  • This study is the first to demonstrate that Aβ and tau accumulation alter synaptic transmission and cortical network hyperexcitability in humans.
  • iNPH biopsies serve as a valuable model for understanding how AD pathology affects neuronal network function.
  • Findings highlight the potential of iNPH tissue for unraveling early AD pathogenesis.