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Alzheimer's disease – because β-amyloid cannot distinguish neurons from bacteria: an in silico simulation study.

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Title: Alzheimer's disease – because β-amyloid cannot distinguish neurons from bacteria: an in silico simulation study.
Authors: Neal, Mathew P.1,2 (AUTHOR), Weaver, Donald F.1,2 (AUTHOR) donald.weaver@utoronto.ca
Source: Pure & Applied Chemistry. Nov2025, Vol. 97 Issue 11, p1667-1674. 8p.
Subjects: Alzheimer's disease, Amyloid beta-protein, Neurons, Bacterial cells, Pathogenesis, Molecular dynamics, Antimicrobial peptides, Molecular physics
Abstract: Based on semi-empirical quantum mechanics calculations and extensive molecular mechanics calculations and molecular dynamics simulations, a novel molecular level conceptualization of key biochemical events in the pathogenesis of Alzheimer's disease (AD) is presented. In response to immune stimulating events (e.g., infection, trauma), β-amyloid (Aβ) protein is released in brain as a protective immunopeptide triggering an immunity cascade in which Aβ exhibits antimicrobial activity, which mistakenly results in a misdirected attack upon "self" neurons, arising from the macromolecular and electrochemical similarities between neurons and bacteria in terms of transmembrane potential gradients and anionic charge distribution geometries on outer membrane macromolecules (gangliosides in neurons; cardiolipins or lipopolysaccharides in bacteria). Molecular mechanics/dynamics calculations are used to demonstrate how the inability of Aβ to distinguish between bacteria and neurons is a central pathological process in the pathogenesis of AD. [ABSTRACT FROM AUTHOR]
Copyright of Pure & Applied Chemistry is the property of De Gruyter 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.)
Database: Engineering Source
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DbLabel: Engineering Source
An: 189572973
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PubType: Academic Journal
PubTypeId: academicJournal
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  Label: Title
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  Data: Alzheimer's disease – because β-amyloid cannot distinguish neurons from bacteria: an in silico simulation study.
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  Data: <searchLink fieldCode="AR" term="%22Neal%2C+Mathew+P%2E%22">Neal, Mathew P.</searchLink><relatesTo>1,2</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Weaver%2C+Donald+F%2E%22">Weaver, Donald F.</searchLink><relatesTo>1,2</relatesTo> (AUTHOR)<i> donald.weaver@utoronto.ca</i>
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  Data: <searchLink fieldCode="JN" term="%22Pure+%26+Applied+Chemistry%22">Pure & Applied Chemistry</searchLink>. Nov2025, Vol. 97 Issue 11, p1667-1674. 8p.
– Name: Subject
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  Data: <searchLink fieldCode="DE" term="%22Alzheimer's+disease%22">Alzheimer's disease</searchLink><br /><searchLink fieldCode="DE" term="%22Amyloid+beta-protein%22">Amyloid beta-protein</searchLink><br /><searchLink fieldCode="DE" term="%22Neurons%22">Neurons</searchLink><br /><searchLink fieldCode="DE" term="%22Bacterial+cells%22">Bacterial cells</searchLink><br /><searchLink fieldCode="DE" term="%22Pathogenesis%22">Pathogenesis</searchLink><br /><searchLink fieldCode="DE" term="%22Molecular+dynamics%22">Molecular dynamics</searchLink><br /><searchLink fieldCode="DE" term="%22Antimicrobial+peptides%22">Antimicrobial peptides</searchLink><br /><searchLink fieldCode="DE" term="%22Molecular+physics%22">Molecular physics</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: Based on semi-empirical quantum mechanics calculations and extensive molecular mechanics calculations and molecular dynamics simulations, a novel molecular level conceptualization of key biochemical events in the pathogenesis of Alzheimer's disease (AD) is presented. In response to immune stimulating events (e.g., infection, trauma), β-amyloid (Aβ) protein is released in brain as a protective immunopeptide triggering an immunity cascade in which Aβ exhibits antimicrobial activity, which mistakenly results in a misdirected attack upon "self" neurons, arising from the macromolecular and electrochemical similarities between neurons and bacteria in terms of transmembrane potential gradients and anionic charge distribution geometries on outer membrane macromolecules (gangliosides in neurons; cardiolipins or lipopolysaccharides in bacteria). Molecular mechanics/dynamics calculations are used to demonstrate how the inability of Aβ to distinguish between bacteria and neurons is a central pathological process in the pathogenesis of AD. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
  Label:
  Group: Ab
  Data: <i>Copyright of Pure & Applied Chemistry is the property of De Gruyter 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:
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    Identifiers:
      – Type: doi
        Value: 10.1515/pac-2025-0471
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      – Code: eng
        Text: English
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        PageCount: 8
        StartPage: 1667
    Subjects:
      – SubjectFull: Alzheimer's disease
        Type: general
      – SubjectFull: Amyloid beta-protein
        Type: general
      – SubjectFull: Neurons
        Type: general
      – SubjectFull: Bacterial cells
        Type: general
      – SubjectFull: Pathogenesis
        Type: general
      – SubjectFull: Molecular dynamics
        Type: general
      – SubjectFull: Antimicrobial peptides
        Type: general
      – SubjectFull: Molecular physics
        Type: general
    Titles:
      – TitleFull: Alzheimer's disease – because β-amyloid cannot distinguish neurons from bacteria: an in silico simulation study.
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            NameFull: Neal, Mathew P.
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            NameFull: Weaver, Donald F.
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            – D: 01
              M: 11
              Text: Nov2025
              Type: published
              Y: 2025
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            – TitleFull: Pure & Applied Chemistry
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