Kinases and Phosphatases in Alzheimer's Disease
A Special Issue of Kinases and Phosphatases (ISSN 2813-3757).
Deadline for manuscript submissions: 30 December 2026 | Viewed by 594
Editor
2. Clinical University Hospital (CHUS), SERGAS, Travesía da Choupana, S/N, Santiago de Compostela, 15706 A Coruña, Spain
Interests: sphingolipids; cancer; inflammation; signaling pathways; neurosciences; Alzheimer’s disease; memory
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Protein phosphorylation is a central mechanism regulating neuronal function, synaptic plasticity, and survival. In Alzheimer’s disease (AD), dysregulation of kinases and phosphatases critically contributes to the abnormal phosphorylation of tau, the dysfunction of amyloid precursor protein processing, and neuroinflammatory signaling. Numerous kinases, including glycogen synthase kinase-3β (GSK-3β), cyclin-dependent kinase 5 (CDK5), and mitogen-activated protein kinases (MAPKs), drive hyperphosphorylation of tau and other neuronal substrates, while the reduced activity of key phosphatases such as protein phosphatase 2A (PP2A) exacerbates tau pathology and synaptic loss.
Emerging evidence reveals that this dysregulation extends beyond neurons to glial cells and the neurovascular unit. In astrocytes and microglia, kinases and phosphatases modulate inflammatory cascades, cytokine release, and synaptic pruning. Similarly, endothelial and pericytic signaling through kinases such as Src, protein kinase B (also known as AKT), and Adenosine Monophosphate-Activated Protein Kinase (AMPK) influences blood–brain barrier (BBB) integrity, vascular inflammation, and transport of neurotoxic proteins. These interconnected processes highlight the central role of phospho-signaling in shaping the neuron–glia–vascular triad that determines AD progression.
This Special Issue seeks to bring together studies investigating the roles of kinases and phosphatases in neuronal, glial, and vascular compartments of the brain in AD and related tauopathies. We welcome research exploring molecular mechanisms, multi-omics analyses, translational models, and therapeutic interventions targeting kinase/phosphatase pathways to restore phospho-homeostasis and preserve brain connectivity and barrier function.
Dr. Alberto Ouro
Guest Editor
Manuscript Submission Information
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Keywords
- Alzheimer’s disease
- kinases
- phosphatases
- tau phosphorylation
- GSK-3β
- CDK5
- PP2A
- glia
- astrocytes
- microglia
- blood–brain barrier
- neuroinflammation
- neurovascular unit
- therapeutic targets
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