Bayesian modelling of amyloid-beta dynamics and astrocyte influence in Alzheimer's disease.

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Title: Bayesian modelling of amyloid-beta dynamics and astrocyte influence in Alzheimer's disease.
Authors: Shaheen, Hina1 (AUTHOR) hina.shaheen@umanitoba.ca, Melnik, Roderick2 (AUTHOR) rmelnik@wlu.ca
Source: Journal of Neuroscience Methods. Sep2026, Vol. 433, pN.PAG-N.PAG. 1p.
Subjects: Amyloid beta-protein, Astrocytes, Stochastic models, Medical model, Alzheimer's disease, Bayesian analysis, Neurodegeneration
Abstract: Alzheimer's disease (AD) is a complicated neurological condition defined by the deposition of amyloid-beta (A β) plaques. Despite extensive research, the dynamics of A β growth, particularly the role of astrocytes, remain poorly understood, limiting the development of effective treatments. This study addresses this gap by introducing a Bayesian inference framework for modelling A β dynamics, incorporating both strong and weak astrocyte effects utilizing Alzheimer's Disease Neuroimaging Initiative (ADNI) clinical data. Through a combination of stochastic growth models and approximate Bayesian computation (ABC), we evaluate how astrocyte concentrations influence A β accumulation in different disease stages. Our findings show that higher astrocyte levels can suppress A β growth, while lower levels promote it, suggesting that astrocyte-targeted interventions may alter disease progression. This data-driven probabilistic approach not only captures the inherent biological variability but also provides a tractable method to estimate uncertain parameters. The present research offers a valuable tool for therapeutic modelling and prediction in AD. • Develops a Bayesian stochastic modelling framework for amyloid-beta (A β) dynamics in Alzheimer's disease using longitudinal ADNI data and Approximate Bayesian Computation (ABC) for likelihood-free parameter inference. • Incorporates astrocyte-mediated effects through threshold-based stochastic models and compares multiple formulations (sM1–sM3) to investigate their role in disease progression. • Demonstrates that astrocyte-dependent stochastic models better capture observed Alzheimer's disease progression trends compared with baseline formulations. • Provides a data-driven computational framework integrating biological mechanisms, stochastic modelling, and Bayesian inference for studying neurodegenerative processes. • Discusses current model limitations and outlines future directions, including multi-state astrocyte modelling and extension to early-stage disease dynamics. [ABSTRACT FROM AUTHOR]
Copyright of Journal of Neuroscience Methods is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Data: Bayesian modelling of amyloid-beta dynamics and astrocyte influence in Alzheimer's disease.
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  Data: <searchLink fieldCode="AR" term="%22Shaheen%2C+Hina%22">Shaheen, Hina</searchLink><relatesTo>1</relatesTo> (AUTHOR)<i> hina.shaheen@umanitoba.ca</i><br /><searchLink fieldCode="AR" term="%22Melnik%2C+Roderick%22">Melnik, Roderick</searchLink><relatesTo>2</relatesTo> (AUTHOR)<i> rmelnik@wlu.ca</i>
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  Data: <searchLink fieldCode="JN" term="%22Journal+of+Neuroscience+Methods%22">Journal of Neuroscience Methods</searchLink>. Sep2026, Vol. 433, pN.PAG-N.PAG. 1p.
– Name: Subject
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  Data: <searchLink fieldCode="DE" term="%22Amyloid+beta-protein%22">Amyloid beta-protein</searchLink><br /><searchLink fieldCode="DE" term="%22Astrocytes%22">Astrocytes</searchLink><br /><searchLink fieldCode="DE" term="%22Stochastic+models%22">Stochastic models</searchLink><br /><searchLink fieldCode="DE" term="%22Medical+model%22">Medical model</searchLink><br /><searchLink fieldCode="DE" term="%22Alzheimer's+disease%22">Alzheimer's disease</searchLink><br /><searchLink fieldCode="DE" term="%22Bayesian+analysis%22">Bayesian analysis</searchLink><br /><searchLink fieldCode="DE" term="%22Neurodegeneration%22">Neurodegeneration</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: Alzheimer's disease (AD) is a complicated neurological condition defined by the deposition of amyloid-beta (A β) plaques. Despite extensive research, the dynamics of A β growth, particularly the role of astrocytes, remain poorly understood, limiting the development of effective treatments. This study addresses this gap by introducing a Bayesian inference framework for modelling A β dynamics, incorporating both strong and weak astrocyte effects utilizing Alzheimer's Disease Neuroimaging Initiative (ADNI) clinical data. Through a combination of stochastic growth models and approximate Bayesian computation (ABC), we evaluate how astrocyte concentrations influence A β accumulation in different disease stages. Our findings show that higher astrocyte levels can suppress A β growth, while lower levels promote it, suggesting that astrocyte-targeted interventions may alter disease progression. This data-driven probabilistic approach not only captures the inherent biological variability but also provides a tractable method to estimate uncertain parameters. The present research offers a valuable tool for therapeutic modelling and prediction in AD. • Develops a Bayesian stochastic modelling framework for amyloid-beta (A β) dynamics in Alzheimer's disease using longitudinal ADNI data and Approximate Bayesian Computation (ABC) for likelihood-free parameter inference. • Incorporates astrocyte-mediated effects through threshold-based stochastic models and compares multiple formulations (sM1–sM3) to investigate their role in disease progression. • Demonstrates that astrocyte-dependent stochastic models better capture observed Alzheimer's disease progression trends compared with baseline formulations. • Provides a data-driven computational framework integrating biological mechanisms, stochastic modelling, and Bayesian inference for studying neurodegenerative processes. • Discusses current model limitations and outlines future directions, including multi-state astrocyte modelling and extension to early-stage disease dynamics. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
  Label:
  Group: Ab
  Data: <i>Copyright of Journal of Neuroscience Methods is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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RecordInfo BibRecord:
  BibEntity:
    Identifiers:
      – Type: doi
        Value: 10.1016/j.jneumeth.2026.110785
    Languages:
      – Code: eng
        Text: English
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        PageCount: 1
        StartPage: N.PAG
    Subjects:
      – SubjectFull: Amyloid beta-protein
        Type: general
      – SubjectFull: Astrocytes
        Type: general
      – SubjectFull: Stochastic models
        Type: general
      – SubjectFull: Medical model
        Type: general
      – SubjectFull: Alzheimer's disease
        Type: general
      – SubjectFull: Bayesian analysis
        Type: general
      – SubjectFull: Neurodegeneration
        Type: general
    Titles:
      – TitleFull: Bayesian modelling of amyloid-beta dynamics and astrocyte influence in Alzheimer's disease.
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      – PersonEntity:
          Name:
            NameFull: Shaheen, Hina
      – PersonEntity:
          Name:
            NameFull: Melnik, Roderick
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          Dates:
            – D: 01
              M: 09
              Text: Sep2026
              Type: published
              Y: 2026
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              Value: 433
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            – TitleFull: Journal of Neuroscience Methods
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