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Pathophysiology
Volume 33
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10.3390/pathophysiology33010014
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Review

Amyloid Beta Oligomers as Early Triggers of Neuronal Cytoskeleton Dysfunction in Alzheimer’s Disease

by
Yadira Gasca-Martínez
1,
Miguel Angel Ontiveros-Torres
2,
Isaías López-Gallegos
1 and
José Jaime Jarero-Basulto
1,*
1
Departamento de Biología Celular y Molecular, Universidad de Guadalajara, Zapopan 45200, Jalisco, Mexico
2
Escuela de Ingeniería y Ciencias, Tecnológico de Monterrey, Monterrey 64849, Nuevo León, Mexico
*
Author to whom correspondence should be addressed.
Pathophysiology 2026, 33(1), 14; https://doi.org/10.3390/pathophysiology33010014
Submission received: 18 December 2025 / Revised: 24 January 2026 / Accepted: 29 January 2026 / Published: 3 February 2026
(This article belongs to the Section Neurodegenerative Disorders)
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Abstract

Alzheimer’s disease (AD) is characterized by progressive cognitive decline, with amyloid beta oligomers (AβOs) emerging as the most neurotoxic species and acting as early triggers of cellular alterations. Before the appearance of other protein aggregates, AβOs disrupt the dynamics and stability of the neuronal cytoskeleton, a structure essential for maintaining neuronal morphology, axonal transport, and synaptic plasticity. Experimental evidence demonstrates that AβOs promote microtubule disassembly, Tau hyperphosphorylation, reduced kinesin levels, impaired axonal transport, and alterations in actin dynamics through the LIMK–cofilin signaling pathway. In addition, increased levels of neurofilament light chain have been identified as an early biomarker of axonal damage. Notably, these cytoskeletal disturbances arise in the absence of extensive neuronal death, underscoring the cytoskeleton as a critical early target in AD pathogenesis. In this review, we analyze cytoskeletal alterations induced by AβOs in neurons and discuss how these changes may contribute to disrupted neuronal communication, a defining early hallmark of AD pathology.
Keywords: Alzheimer’s disease; amyloid beta; oligomers; aggregates; cytoskeleton Alzheimer’s disease; amyloid beta; oligomers; aggregates; cytoskeleton
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MDPI and ACS Style

Gasca-Martínez, Y.; Ontiveros-Torres, M.A.; López-Gallegos, I.; Jarero-Basulto, J.J. Amyloid Beta Oligomers as Early Triggers of Neuronal Cytoskeleton Dysfunction in Alzheimer’s Disease. Pathophysiology 2026, 33, 14. https://doi.org/10.3390/pathophysiology33010014

AMA Style

Gasca-Martínez Y, Ontiveros-Torres MA, López-Gallegos I, Jarero-Basulto JJ. Amyloid Beta Oligomers as Early Triggers of Neuronal Cytoskeleton Dysfunction in Alzheimer’s Disease. Pathophysiology. 2026; 33(1):14. https://doi.org/10.3390/pathophysiology33010014

Chicago/Turabian Style

Gasca-Martínez, Yadira, Miguel Angel Ontiveros-Torres, Isaías López-Gallegos, and José Jaime Jarero-Basulto. 2026. "Amyloid Beta Oligomers as Early Triggers of Neuronal Cytoskeleton Dysfunction in Alzheimer’s Disease" Pathophysiology 33, no. 1: 14. https://doi.org/10.3390/pathophysiology33010014

APA Style

Gasca-Martínez, Y., Ontiveros-Torres, M. A., López-Gallegos, I., & Jarero-Basulto, J. J. (2026). Amyloid Beta Oligomers as Early Triggers of Neuronal Cytoskeleton Dysfunction in Alzheimer’s Disease. Pathophysiology, 33(1), 14. https://doi.org/10.3390/pathophysiology33010014

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