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Peer-reviewedCC BYCellular and molecular neurobiology

Glutamate, Immune Cells and Alzheimer's Disease: An Attempt to Link the Triad.

  • Nikolaos A Chinas1,2
  • Harry Alexopoulos3
  1. 1Department of Cell Biology and Biophysics, Faculty of Biology, National and Kapodistrian University of Athens, Athens, Greece. [email protected].
  2. 2Department of Genetics, Microbiology and Statistics, Institut de Biomedicina de la Universitat de Barcelona (IBUB), Universitat de Barcelona, Barcelona, Spain. [email protected].
  3. 3Department of Cell Biology and Biophysics, Faculty of Biology, National and Kapodistrian University of Athens, Athens, Greece. [email protected].
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Abstract

Glutamate (Glu), although the main excitatory neurotransmitter (NT) of the central nervous system (CNS), evidence recognizes its role in influencing immune cell function and activation, including cytokine production, cell proliferation, migration, and survival. Importantly, dysregulation of Glu homeostasis has been implicated in the pathogenesis of Alzheimer's disease (AD), a neurodegenerative disorder characterized by progressive cognitive decline, neuronal loss and neuroinflammation. This review synthesizes current evidence on the biochemistry of the glutamatergic synapse, as well as the expression and signaling of Glu receptors (GluRs) in human immune cells. Furthermore, it examines two major hypotheses of AD pathogenesis -the glutamatergic and the neuroimmune hypothesis- and proposes a unified glutamatergic-neuroimmune framework. In this model, disrupted glutamatergic signaling at the neuron-glia-immune interface may represent a central contributor to AD pathology. Understanding the glutamatergic-neuroimmune axis may provide novel insights into therapeutic strategies targeting neuroimmune modulation in AD.

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Cite

BibTeXRIS
BibTeX
@article{chinas2026glutamate,
  title = {{Glutamate, Immune Cells and Alzheimer's Disease: An Attempt to Link the Triad.}},
  author = {Nikolaos A Chinas and Harry Alexopoulos},
  journal = {Cellular and molecular neurobiology},
  year = {2026},
  month = jul,
  doi = {10.1007/s10571-026-01784-w},
  url = {https://europepmc.org/article/MED/42909691},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Glutamate, Immune Cells and Alzheimer's Disease: An Attempt to Link the Triad.
AU  - Nikolaos A Chinas
AU  - Harry Alexopoulos
PY  - 2026
DA  - 2026/07/28
JO  - Cellular and molecular neurobiology
DO  - 10.1007/s10571-026-01784-w
UR  - https://europepmc.org/article/MED/42909691
AB  - Glutamate (Glu), although the main excitatory neurotransmitter (NT) of the central nervous system (CNS), evidence recognizes its role in influencing immune cell function and activation, including cytokine production, cell proliferation, migration, and survival. Importantly, dysregulation of Glu homeostasis has been implicated in the pathogenesis of Alzheimer's disease (AD), a neurodegenerative disorder characterized by progressive cognitive decline, neuronal loss and neuroinflammation. This review synthesizes current evidence on the biochemistry of the glutamatergic synapse, as well as the expression and signaling of Glu receptors (GluRs) in human immune cells. Furthermore, it examines two major hypotheses of AD pathogenesis -the glutamatergic and the neuroimmune hypothesis- and proposes a unified glutamatergic-neuroimmune framework. In this model, disrupted glutamatergic signaling at the neuron-glia-immune interface may represent a central contributor to AD pathology. Understanding the glutamatergic-neuroimmune axis may provide novel insights into therapeutic strategies targeting neuroimmune modulation in AD.
SN  - 0272-4340
SN  - 1573-6830
ER  -