TDP43 pathology in chronic traumatic encephalopathy retinas.

Autor: Phansalkar R; School of Medicine, Stanford University, Stanford, CA, USA., Goodwill VS; Department of Pathology, University of California, San Diego, La Jolla, CA, USA., Nirschl JJ; Departments of Ophthalmology and Pathology, Stanford University, Stanford, CA, USA., De Lillo C; Vita-Salute San Raffaele University, Milan, Italy., Choi J; The University of Texas Southwestern Medical Center, Dallas, TX, USA., Spurlock E; Boston University Alzheimer's Disease and CTE Center, Boston University School of Medicine, Boston, MA, USA., Coughlin DG; Department of Neurosciences, University of California, San Diego, La Jolla, CA, USA., Pizzo D; Department of Pathology, University of California, San Diego, La Jolla, CA, USA., Sigurdson CJ; Department of Pathology, University of California, San Diego, La Jolla, CA, USA., Hiniker A; Department of Pathology, University of California, San Diego, La Jolla, CA, USA., Alvarez VE; Boston University Alzheimer's Disease and CTE Center, Boston University School of Medicine, Boston, MA, USA.; VA Boston Healthcare System, Boston, MA, USA., Mckee AC; Boston University Alzheimer's Disease and CTE Center, Boston University School of Medicine, Boston, MA, USA.; VA Boston Healthcare System, Boston, MA, USA., Lin JH; Departments of Ophthalmology and Pathology, Stanford University, Stanford, CA, USA. Jonathan.H.Lin@stanford.edu.; VA Palo Alto Healthcare System, Palo Alto, CA, USA. Jonathan.H.Lin@stanford.edu.
Jazyk: angličtina
Zdroj: Acta neuropathologica communications [Acta Neuropathol Commun] 2023 Sep 22; Vol. 11 (1), pp. 152. Date of Electronic Publication: 2023 Sep 22.
DOI: 10.1186/s40478-023-01650-6
Abstrakt: Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease associated with repetitive head trauma. Brain pathology in CTE is characterized by neuronal loss, gliosis, and a distinctive pattern of neuronal accumulation of hyper-phosphorylated tau (p-tau) and phospho-TDP43 (p-TDP43). Visual anomalies have been reported by patients with CTE, but the ocular pathology underlying these symptoms is unknown. We evaluated retinal pathology in post-mortem eyes collected from 8 contact sport athletes with brain autopsy-confirmed stage IV CTE and compared their findings to retinas from 8 control patients without CTE and with no known history of head injury. Pupil-optic nerve cross sections were prepared and stained with hematoxylin and eosin (H&E), p-tau, p-TDP43, and total TDP43 by immunohistochemistry. No significant retinal degeneration was observed in CTE eyes compared to control eyes by H&E. Strong cytoplasmic p-TDP43 and total TDP43 staining was found in 6/8 CTE eyes in a subset of inner nuclear layer interneurons (INL) of the retina, while only 1/8 control eyes showed similar p-TDP43 pathology. The morphology and location of these inner nuclear layer interneurons were most compatible with retinal horizontal cells, although other retinal cell types present in INL could not be ruled out. No p-tau pathology was observed in CTE or control retinas. These findings identify novel retinal TDP43 pathology in CTE retinas and support further investigation into the role of p-TDP43 in producing visual deficits in patients with CTE.
(© 2023. BioMed Central Ltd., part of Springer Nature.)
Databáze: MEDLINE
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