ArticleMovement disorders : official journal of the Movement Disorder Society2017
Distribution and characteristics of transactive response DNA binding protein 43 kDa pathology in progressive supranuclear palsy.
Article in Movement disorders : official journal of the Movement Disorder Society, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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44 citing papers in PubMed, 61 citations in OpenAlex.
- TDP-43: [GU]-ardian of the transcriptome.Molecular neurodegeneration · 2026Review
- Comorbid pathologies and their impact on progressive supranuclear palsy: current view.Journal of neural transmission (Vienna, Austria : 1996) · 2026Review
- Targeting protein aggregate co-pathologies in neurodegeneration: a viable therapeutic strategy?Molecular neurodegeneration advances · 2026Review
- Nanoparticles of non-porphyrinic covalent organic frameworks as contrast agents for photoacoustic imaging.Scientific reports · 2025Article
- Frontotemporal Lobar degeneration with TDP-43 presenting as progressive supranuclear palsy syndrome.Acta neuropathologica communications · 2025Article
- Looking into Abnormal Co-Expressions of Tau and TDP-43 in the Realm of Mixed Dementia Types: A Double-Punch Scenario.Brain sciences · 2025Review
- A 15-Item modification of the PSP rating scale to improve clinical meaningfulness and statistical performance.Nature communications · 2025Article
- TDP-43-proteinopathy at the crossroads of tauopathy: on copathology and current and prospective biomarkers.Frontiers in cellular neuroscience · 2025Review
- Decoding TDP-43: the molecular chameleon of neurodegenerative diseases.Acta neuropathologica communications · 2024Review
- Co-Aggregation of TDP-43 with Other Pathogenic Proteins and Their Co-Pathologies in Neurodegenerative Diseases.International journal of molecular sciences · 2024Review
- Limbic-predominant age-related TDP-43 encephalopathy (LATE-NC): Co-pathologies and genetic risk factors provide clues about pathogenesis.Journal of neuropathology and experimental neurology · 2024Review
- Clinicopathologic features of a novel star-shaped transactive response DNA-binding protein 43 (TDP-43) pathology in the oldest old.Journal of neuropathology and experimental neurology · 2023Article
- Interaction of Proteins Involved in Neuronal Proteinopathies.Life (Basel, Switzerland) · 2023Review
- The frequency and distribution of TDP-43 pathology in argyrophilic grain disease.Journal of neuropathology and experimental neurology · 2023Article
- Cerebral Tau Deposition in Comorbid Progressive Supranuclear Palsy and Amyotrophic Lateral Sclerosis: An [18F]-Flortaucipir and 7T MRI Study.Neuro-degenerative diseases · 2023Article
- TDP-43 Proteinopathy and Tauopathy: Do They Have Pathomechanistic Links?International journal of molecular sciences · 2022Review
- Molecular Dissection of TDP-43 as a Leading Cause of ALS/FTLD.International journal of molecular sciences · 2022Review
- Frontotemporal lobar degeneration with TAR DNA-binding protein 43 (TDP-43): its journey of more than 100 years.Journal of neurology · 2022Review
- The Role of TDP-43 in Neurodegenerative Disease.Molecular neurobiology · 2022Review
- Concurrent tau pathologies in frontotemporal lobar degeneration with TDP-43 pathology.Neuropathology and applied neurobiology · 2022Article
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10 authors at 2 institutions in 1 country.
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Abstract
backgroundThis study aimed to determine the frequency of transactive response DNA binding protein 43 kDa pathology in PSP, the clinical features of patients with this pathology, and genetic risk factors for it.
methodsHippocampal sections were screened with immunohistochemistry for transactive response DNA binding protein 43 kDa in 945 PSP cases. A subset of 261 cases that were negative in hippocampus was screened in the amygdala. The density and disruption of this pathology, as well as regional tau burden, and clinical and genetic characteristics were analyzed.
resultsWe observed transactive response DNA binding protein 43 kDa pathology in 47 cases in the hippocampus and an additional 9 cases that only affected the amygdala. Hippocampal sclerosis was the strongest risk factor, followed by Alzheimer's disease pathology, argyrophilic grain disease, and older age at death. Five stages of transactive response DNA binding protein 43 kDa pathology were identified in PSP: Stage A had pathology only in the amygdala (16%); stage I had pathology confined to the hippocampus and entorhinal cortex (9%); stage II included both regions of stage A and I (38%); stage III spread further to medial occipitotemporal gyrus (20%); and stage IV had pathology in the dorsolateral frontal lobe (18%). Anatomical areas vulnerable to PSP pathology had varying degrees of this pathology in stage II and later. PSP with transactive response DNA binding protein 43 kDa pathology were older at disease onset and had lower median MMSE scores; however, the latter was driven by concurrent pathologies.
conclusionsDistribution and clinical characteristics of transactive response DNA binding protein 43 kDa pathology in PSP were influenced by concurrent pathologies. This is the first study to observe that PSP-vulnerable regions are also susceptible to this non-tau pathology. © 2016 International Parkinson and Movement Disorder Society.
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