ReviewCurrent neuropharmacology2026
Protein Kinases in Alzheimer's Disease: Pioneering Insights into Pathogenesis and Therapeutic Breakthroughs.
Review in Current neuropharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- Alzheimer's disease: disrupted communication between the endoplasmic reticulum and mitochondria.Journal of neurology · 2026Review
- Advances in the treatment of Alzheimer's disease.Frontiers in pharmacology · 2026Review
- Osteoimmuno-brain axis: a bridge connecting osteoporosis and cognitive decline and its clinical significance in dementia and Alzheimer's disease.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's Disease (AD) is an exhausting neurodegenerative condition marked by the build-up of abnormal protein aggregates in the brain and a progressive loss of cognitive function. The complicated role that protein kinases play in the pathophysiology of AD has come to light more and more in recent years. The symptoms of AD include memory loss, cognitive impairment, and neuronal malfunction. Many cellular processes, including synaptic plasticity, neuronal survival, and protein homeostasis, have been linked to protein kinases, a class of enzymes that control phosphorylation. The etiology of AD has been closely related to the dysregulation of protein kinases, including those implicated in the phosphorylation of tau and the formation of amyloid-beta. GSK-3, also known as glycogen synthase kinase, is one of the most studied protein kinases in Alzheimer's disease. It is known that GSK-3 phosphorylates tau protein, causing it to clump together and create neurofibrillary tangles. Moreover, GSK-3 activation increases the development of amyloid-beta, which furthers the disease's progression. Additional protein kinases, including Cyclin-Dependent Kinase 5 (CDK5) and calcium/calmodulin-dependent protein kinase II (CaMKII), have also been connected to tau phosphorylation and synaptic dysfunction in AD. Protein kinases play a crucial role in the pathophysiology of AD, extending beyond tau phosphorylation. Research has shown that Amyloid Precursor Protein (APP) processing is regulated by Protein Kinases A (PKA) and C (PKC), which affects the production and clearance of amyloid-beta. Furthermore, AD etiology involves oxidative stress, neuroinflammation, and mitochondrial dysfunction, all of which are regulated by protein kinases. This study will cover the effects of protein kinases in AD, focusing on their role in tau phosphorylation, an attribute of the disease. We will also address the role of protein kinase in the development of amyloid-beta, synaptic malfunction, and neuroinflammation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.