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Related Experiment Video

Updated: Jan 16, 2026

Preparation of Oligomeric β-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices

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Pathological calcium influx through amyloid beta pores disrupts synaptic function.

Temitope Adeoye¹, Ghanim Ullah¹

¹Department of Physics, University of South Florida, Tampa, FL 33620, USA.

|October 5, 2025

Summary

Alzheimer's disease (AD) involves amyloid-beta (Aβ) oligomers disrupting calcium (Ca2+) homeostasis. This study models how Aβ pores alter synaptic transmission, revealing complex effects on neurotransmitter release and interactions with ER dysfunction in AD.

Keywords:

Alzheimer’s disease Amyloid beta pores Asynchronous release Neuronal calcium signalling Neurotransmitter release Synchronous release

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Area of Science:

Neuroscience
Computational Biology
Cell Biology

Background:

Alzheimer's disease (AD) is linked to synaptic dysfunction and amyloid-beta (Aβ) oligomers disrupting calcium (Ca2+) homeostasis via membrane pores.
The precise impact of these Aβ pores on synaptic transmission and their interaction with Familial AD (FAD)-associated endoplasmic reticulum (ER) dysfunction are not fully understood.

Purpose of the Study:

To model how Aβ pores affect presynaptic Ca2+ dynamics, exocytosis, and neurotransmitter release.
To investigate the combined effects of Aβ pores and FAD-associated ER dysfunction on synaptic function.

Main Methods:

Extended a pre-existing computational model of presynaptic Ca2+ dynamics.
Simulated the impact of Aβ pores with varying activity patterns on neurotransmitter release.
Analyzed the interplay between Aβ pores and ER Ca2+ dysregulation.

Main Results:

Aβ pores significantly alter neurotransmitter release timing and strength.
Continuous pore activity causes synaptic hyperactivation; brief intense activity leads to lasting hypoactivation.
Aβ pores and ER dysfunction interact synergistically, creating complex Ca2+ disruptions and altering release patterns, particularly asynchronous release.

Conclusions:

Aβ pores fundamentally disrupt synaptic function, with effects dependent on their activity patterns.
The interplay between Aβ pores and ER dysfunction creates a pathological unit exacerbating synaptic failure.
Early synaptic dysfunction in AD may stem from temporal release coordination issues rather than solely Ca2+ dysregulation.