Evidence map›Paper›PMID 41868623›Full record

ArticleFrontiers in dementia2026

Amyloid-β acute exposition affects the CA1 hippocampal network activity and its topological organization, evaluated with multielectrode arrays.

David Alcantara-Gonzalez, Elizabeth Santiago, Fernando Peña-Ortega

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Article in Frontiers in dementia, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

3 authors.

David Alcantara-GonzalezDepartamento de Neurobiología del Desarrollo y Neurofisiología, Instituto de Neurobiología, Universidad Nacional Autónoma de México, Querétaro, Mexico.
Elizabeth SantiagoDepartamento de Neurobiología del Desarrollo y Neurofisiología, Instituto de Neurobiología, Universidad Nacional Autónoma de México, Querétaro, Mexico.
Fernando Peña-OrtegaDepartamento de Neurobiología del Desarrollo y Neurofisiología, Instituto de Neurobiología, Universidad Nacional Autónoma de México, Querétaro, Mexico.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Neuronal networks enable brain's information processing through a well-coordinated activity. Disruptions in this activity can impair key brain functions such as synaptic plasticity and long-term memory. Such dysfunctions are relevant to the cognitive deterioration in Alzheimer's disease (AD). Neuronal circuit alterations in AD are associated with amyloid-β (Aβ) extracellular accumulation across multiple brain regions involved in cognitive regulation. Although several studies have analyzed network topology and examined anatomical, functional, and effective connectivity to understand their role in AD, the direct contribution of Aβ to local neuronal network disturbances has not been investigated. Methods: We assessed the CA1 hippocampal network structure after acute exposure to Aβ1-42 (30 nM) using an Results: CA1 hippocampal neurons showed an average reduced firing frequency. However, some putative pyramidal neurons and interneurons increased their activity. These differences in activity are cell-type-specific, being the interneurons the cells that mainly reduce their firing in presence of Aβ. The number and magnitude of their functional links within the network were not different, but a synchronized firing pattern of different neurons was observed. These changes were associated with alterations to the network's topological structure, indicating the generation of highly connected nodes in the presence of Aβ. Conclusion: The main change in the reconfiguration of the CA1 hippocampal network induced by acute exposure to Aβ involved the differential change in firing of different neurons, where the average reduction in firing was found, but some neurons increased their firing. This may constitute an adaptive mechanisms that compensate for neuronal connectivity and help maintain the level of activity. This is the first time the Estrada index has been used to elucidate alterations in the topological neuronal network in an

Indexed as

Alzheimer’s diseaseamyloid-βEstrada indexhippocampal sliceshyperexcitabilityneuronal networksneuronal network topology

Identifiers

PMID41868623
PMCPMC13002378

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