ArticleMolecular neurobiology2020
Beta-Amyloid Increases the Expression Levels of Tid1 Responsible for Neuronal Cell Death and Amyloid Beta Production.
Article in Molecular neurobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 21 citations in OpenAlex.
- Mitochondrial dysfunction and programmed cell death in Alzheimer's disease: A retrospective bioinformatics study.Medicine · 2026Article
- Mutual reinforcement of lymphotoxin-driven myositis and impaired autophagy in murine muscle.Brain : a journal of neurology · 2025Article
- HSV-1 hijacks mitochondrial dynamics: potential molecular mechanisms linking viral infection to neurodegenerative disorders.Apoptosis : an international journal on programmed cell death · 2025Review
- Regimen on Dnaja3 haploinsufficiency mediated sarcopenic obesity with imbalanced mitochondrial homeostasis and lipid metabolism.Journal of cachexia, sarcopenia and muscle · 2024Article
- Temporal sex specific brain gene expression pattern during early rat embryonic development.Frontiers in cell and developmental biology · 2024Article
- A peptide derived from TID1S rescues frataxin deficiency and mitochondrial defects in FRDA cellular models.Frontiers in pharmacology · 2024Article
- Neuroproteomic Analysis after SARS-CoV-2 Infection Reveals Overrepresented Neurodegeneration Pathways and Disrupted Metabolic Pathways.Biomolecules · 2023Article
- Deletion of UCP1 in Tg2576 Mice Increases Body Temperature and Exacerbates Alzheimer's Disease-Related Pathologies.International journal of molecular sciences · 2023Article
- Co-administration of Nanowired Oxiracetam and Neprilysin with Monoclonal Antibodies to Amyloid Beta Peptide and p-Tau Thwarted Exacerbation of Brain Pathology in Concussive Head Injury at Hot Environment.Advances in neurobiology · 2023Review
- Structural resemblance of the DNAJA-family protein, Tid1, to the DNAJB-family Hsp40.BMB reports · 2022Article
- Insulin Deficiency Increases Sirt2 Level in Streptozotocin-Treated Alzheimer's Disease-Like Mouse Model: Increased Sirt2 Induces Tau Phosphorylation Through ERK Activation.Molecular neurobiology · 2022Article
- Putting human Tid-1 in context: an insight into its role in the cell and in different disease states.Cell communication and signaling : CCS · 2022Review
- Sustained high body temperature exacerbates cognitive function and Alzheimer's disease-related pathologies.Scientific reports · 2022Article
- Recent insights into the role of glia and oxidative stress in Alzheimer's disease gained from Drosophila.Current opinion in neurobiology · 2022Review
- The effect of lipocalin-2 (LCN2) on apoptosis: a proteomics analysis study in an LCN2 deficient mouse model.BMC genomics · 2021Article
- Article
- Forsythoside B attenuates memory impairment and neuroinflammation via inhibition on NF-κB signaling in Alzheimer's disease.Journal of neuroinflammation · 2020Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial dysfunctions and oxidative stress play important roles in the early pathogenesis of Alzheimer's disease (AD), which also involves the aberrant expression levels of mitochondrial proteins. However, the molecular mechanisms underlying the aberrant expression levels of these proteins in the pathogenesis of AD are still not completely understood. Tid1 (DnaJA3/mtHsp40), a mammalian homolog of the Drosophila tumor suppressor Tid56, is reported to induce mitochondrial fragmentation associated with an increase in reactive oxygen species (ROS) levels, resulting in cell death in some cancer cells. However, the involvement of Tid1 in AD pathogenesis is as yet unknown. In this study, we found that the Tid1 protein levels were upregulated in the hippocampus of AD patients and Tg2576 mice. Our in vitro studies showed that Aβ42 increased the expression levels of Tid1 in primary rat cortical neurons. The knockdown of Tid1 protected against neuronal cell death induced by Aβ42, and Tid1-mediated neuronal cell death, was dependent on the increased ROS generation and caspase-3 activity. The overexpression of Tid1 in HEK293-APP cells increased the BACE1 levels, resulting in increased Aβ production. Conversely, Tid1 knockdown in HEK293-APP cells and primary cultured neurons decreased Aβ production through the reduction in the BACE1 levels. We also found that the overexpression of Tid1 activated c-Jun N-terminal kinase (JNK) leading to increased Aβ production. Taken together, our results suggest that upregulated Tid1 levels in the hippocampus of patients with AD and Tg2576 mice induce apoptosis and increase Aβ production, and Tid1 may therefore be a suitable target in therapeutic interventions for AD.
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