ArticleFrontiers in molecular neuroscience2018
Melatonin Mitigates Kainic Acid-Induced Neuronal Tau Hyperphosphorylation and Memory Deficits through Alleviating ER Stress.
Article in Frontiers in molecular neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 40 citations in OpenAlex.
- An Expanded Narrative Review of Neurotransmitters on Alzheimer's Disease: The Role of Therapeutic Interventions on Neurotransmission.Molecular neurobiology · 2025Review
- Brain washing and neural health: role of age, sleep, and the cerebrospinal fluid melatonin rhythm.Cellular and molecular life sciences : CMLS · 2023Review
- Melatonin Can Modulate Neurodegenerative Diseases by Regulating Endoplasmic Reticulum Stress.International journal of molecular sciences · 2023Review
- Multi-Targeting Intranasal Nanoformulation as a Therapeutic for Alzheimer's Disease.Biomolecules · 2023Article
- The potential influence of melatonin on mitochondrial quality control: a review.Frontiers in pharmacology · 2023Review
- Renalase Prevents Renal Fibrosis by Inhibiting Endoplasmic Reticulum Stress and Down-Regulating GSK-3β/Snail Signaling.International journal of medical sciences · 2023Article
- NMDA and AMPA Receptors at Synapses: Novel Targets for Tau and α-Synuclein Proteinopathies.Biomedicines · 2022Review
- Tau Toxicity in Neurodegeneration.Molecular neurobiology · 2022Review
- Melatonin ameliorates tau-related pathology via the miR-504-3p and CDK5 axis in Alzheimer's disease.Translational neurodegeneration · 2022Article
- An Anthranilate Derivative Inhibits Glutamate Release and Glutamate Excitotoxicity in Rats.International journal of molecular sciences · 2022Article
- The Prospective Application of Melatonin in Treating Epigenetic Dysfunctional Diseases.Frontiers in pharmacology · 2022Review
- The role of Cdk5 in neurological disorders.Frontiers in cellular neuroscience · 2022Review
- Melatonin: Regulation of Biomolecular Condensates in Neurodegenerative Disorders.Antioxidants (Basel, Switzerland) · 2021Review
- Asiatic Acid Prevents Cognitive Deficits by Inhibiting Calpain Activation and Preserving Synaptic and Mitochondrial Function in Rats with Kainic Acid-Induced Seizure.Biomedicines · 2021Article
- Berberine Reduces AβFrontiers in pharmacology · 2021Article
- Cellular Mechanisms of Melatonin: Insight from Neurodegenerative Diseases.Biomolecules · 2020Review
- Kainic acid hyperphosphorylates tau via inflammasome activation in MAPT transgenic mice.Aging · 2019Article
- Melatonin in Alzheimer's Disease: A Latent Endogenous Regulator of Neurogenesis to Mitigate Alzheimer's Neuropathology.Molecular neurobiology · 2019Review
- Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kainic acid (KA) exposure causes neuronal degeneration featured by Alzheimer-like tau hyperphosphorylation and memory deficits. Melatonin (Mel) is known to protect hippocampal neurons against KA-induced damage. However, the underlying mechanisms remain elusive. In the current study, we investigated the protective effect of melatonin on KA-induced tau hyperphosphorylation by focusing on endoplasmic reticulum (ER) stress-mediated signaling pathways. By using primary hippocampal neurons and mouse brain, we showed that KA treatment specifically induced ER stress and activated GSK-3β and CDK5, two major kinases responsible for tau phosphorylation. Inhibition of ER stress efficiently inactivated GSK-3β and CDK5. Mechanistically, we found that KA-induced ER stress significantly activated calpain, a calcium-dependent protease. Inhibition of ER stress or calpain leads to the reduction in KA-induced GSK-3β and CDK5 activities and tau phosphorylation. Moreover, GSK-3β or CDK5 inhibition failed to downregulate ER stress efficiently, suggesting that ER stress functions upstream of GSK-3β or CDK5. Notably, our results revealed that melatonin acts against KA-induced neuronal degeneration and tau hyperphosphorylation via easing ER stress, further highlighting the protective role of melatonin in the KA-induced neuronal defects.
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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.