ArticlePloS one2012
Model Hirano bodies protect against tau-independent and tau-dependent cell death initiated by the amyloid precursor protein intracellular domain.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 25 citations in OpenAlex.
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- Beliefs about the factors that motivate prosocial sentiments among people in the privileged class of Pakistan during the COVID-19 pandemic.The Journal of social issues · 2022Article
- Ofloxacin as a Disruptor of Actin Aggresome "Hirano Bodies": A Potential Repurposed Drug for the Treatment of Neurodegenerative Diseases.Frontiers in aging neuroscience · 2020Article
- Tau-mediated Neurodegeneration and Potential Implications in Diagnosis and Treatment of Alzheimer's Disease.Chinese medical journal · 2017Review
- De novo actin polymerization is required for model Hirano body formation in Dictyostelium.Biology open · 2016Article
- Hirano body expression impairs spatial working memory in a novel mouse model.Acta neuropathologica communications · 2014Article
- Hirano bodies differentially modulate cell death induced by tau and the amyloid precursor protein intracellular domain.BMC neuroscience · 2014Article
- A comparative study of the dentate gyrus in hippocampal sclerosis in epilepsy and dementia.Neuropathology and applied neurobiology · 2014Article
- Lipoprotein lipase (LPL) is associated with neurite pathology and its levels are markedly reduced in the dentate gyrus of Alzheimer's disease brains.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2013Article
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Authors and funding
3 authors at 1 institution in 1 country.
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Abstract
The main pathological hallmarks of Alzheimer's disease are amyloid-beta plaques and neurofibrillary tangles, which are primarily composed of amyloid precursor protein (APP) and tau, respectively. These proteins and their role in the mechanism of neurodegeneration have been extensively studied. Hirano bodies are a frequently occurring pathology in Alzheimer's disease as well as other neurodegenerative diseases. However, the physiological role of Hirano bodies in neurodegenerative diseases has yet to be determined. We have established cell culture models to study the role of Hirano bodies in amyloid precursor protein and tau-induced cell death mechanisms. Exogenous expression of APP and either of its c-terminal fragments c31 or Amyloid Precursor Protein Intracellular Domain c58 (AICDc58) enhance cell death. The presence of tau is not required for this enhanced cell death. However, the addition of a hyperphosphorylated tau mimic 352PHPtau significantly increases cell death in the presence of both APP and c31 or AICDc58 alone. The mechanism of cell death induced by APP and its c-terminal fragments and tau was investigated. Fe65, Tip60, p53, and caspases play a role in tau-independent and tau-dependent cell death. In addition, apoptosis was determined to contribute to cell death. The presence of model Hirano bodies protected against cell death, indicating Hirano bodies may play a protective role in neurodegeneration.
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