TY - JOUR
T1 - Primary retinal tauopathy
T2 - A tauopathy with a distinct molecular pattern
AU - Walkiewicz, Grzegorz
AU - Ronisz, Alicja
AU - van Ginderdeuren, Rita
AU - Lemmens, Sophie
AU - Bouwman, Femke H.
AU - Hoozemans, Jeroen J. M.
AU - Morrema, Tjado H. J.
AU - Rozemuller, Annemieke J.
AU - Hart de Ruyter, Frederique J.
AU - de Groef, Lies
AU - Stalmans, Ingeborg
AU - Thal, Dietmar Rudolf
N1 - Funding Information: The authors thank Dr. Peter Davies, Department of Pathology, Albert Einstein College of Medicine, USA, for the gift of the PHF1 (= anti-p-tauS396/S404) and MC-1 (detects the paperclip formation of tau) antibodies. The technical help of Simona Ospitalieri is gratefully acknowledged. The project is funded by Stichting Alzheimer Onderzoek (SAO/FRA 2020/017 [DRT], SAO/FRA 2021/0036 [LDG]), Fonds Wetenschappelijk Onderzoek (Vlaanderen; G0F8516N [DRT], G065721N [DRT]), JPND-2020-568-050 BRAINSTORM (IS, LDG, DRT), and KU-Leuven Internal Funding (C3/20/057 [DRT]). GW received a PhD fellowship from KU Leuven internal funds (DB/21/009/GW). LDG was a senior postdoctoral fellow of Fonds Wetenschappelijk Onderzoek (Vlaanderen) (12I3820N). Funding Information: J.J.M.H. received grants from the Dutch Research Council (ZonMW) and Alzheimer Netherlands; and performed contract research or received grants from Merck, ONO Pharmaceuticals, Janssen Prevention Center, DiscovericBio, AxonNeurosciences, Roche, Genentech, Promis, Denali, FirstBiotherapeutics, and Ensol Biosciences. I.S. received consultancies and research grants from Alcon, Allergan/AbbVie, EyeD, Horus, Mona, Santen, and Laboratoires Théa. D.R.T. received speaker honorary from Biogen (USA); travel reimbursement from UCB (Belgium); and collaborated with Novartis Pharma AG (Switzerland), Probiodrug (Germany), GE HealthCare (UK), and Janssen Pharmaceutical Companies (Belgium). All payments were made to the respective institution. The other authors have nothing to declare. Author disclosures are available in the supporting information . Funding Information: The authors thank Dr. Peter Davies, Department of Pathology, Albert Einstein College of Medicine, USA, for the gift of the PHF1 ( = anti‐p‐tau) and MC‐1 (detects the paperclip formation of tau) antibodies. The technical help of Simona Ospitalieri is gratefully acknowledged. The project is funded by Stichting Alzheimer Onderzoek (SAO/FRA 2020/017 [DRT], SAO/FRA 2021/0036 [LDG]), Fonds Wetenschappelijk Onderzoek (Vlaanderen; G0F8516N [DRT], G065721N [DRT]), JPND‐2020‐568‐050 BRAINSTORM (IS, LDG, DRT), and KU‐Leuven Internal Funding (C3/20/057 [DRT]). GW received a PhD fellowship from KU Leuven internal funds (DB/21/009/GW). LDG was a senior postdoctoral fellow of Fonds Wetenschappelijk Onderzoek (Vlaanderen) (12I3820N). S396/S404 Publisher Copyright: © 2023 The Authors. Alzheimer's & Dementia published by Wiley Periodicals LLC on behalf of Alzheimer's Association.
PY - 2024/1
Y1 - 2024/1
N2 - BACKGROUND: Phosphorylated tau (p-tau) accumulation, a hallmark of Alzheimer's disease (AD), can also be found in the retina. However, it is uncertain whether it is linked to AD or another tauopathy. METHODS: Retinas from 164 individuals, with and without AD, were analyzed for p-tau accumulation and its relationship with age, dementia, and vision impairment. RESULTS: Retinal p-tau pathology showed a consistent pattern with four stages and a molecular composition distinct from that of cerebral tauopathies. The stage of retinal p-tau pathology correlated with age (r = 0.176, P = 0.024) and was associated with AD (odds ratio [OR] 3.193; P = 0.001), and inflammation (OR = 2.605; P = 0.001). Vision impairment was associated with underlying eye diseases (β = 0.292; P = 0.001) and the stage of retinal p-tau pathology (β = 0.192; P = 0.030) in a linear regression model. CONCLUSIONS: The results show the presence of a primary retinal tauopathy that is distinct from cerebral tauopathies.
AB - BACKGROUND: Phosphorylated tau (p-tau) accumulation, a hallmark of Alzheimer's disease (AD), can also be found in the retina. However, it is uncertain whether it is linked to AD or another tauopathy. METHODS: Retinas from 164 individuals, with and without AD, were analyzed for p-tau accumulation and its relationship with age, dementia, and vision impairment. RESULTS: Retinal p-tau pathology showed a consistent pattern with four stages and a molecular composition distinct from that of cerebral tauopathies. The stage of retinal p-tau pathology correlated with age (r = 0.176, P = 0.024) and was associated with AD (odds ratio [OR] 3.193; P = 0.001), and inflammation (OR = 2.605; P = 0.001). Vision impairment was associated with underlying eye diseases (β = 0.292; P = 0.001) and the stage of retinal p-tau pathology (β = 0.192; P = 0.030) in a linear regression model. CONCLUSIONS: The results show the presence of a primary retinal tauopathy that is distinct from cerebral tauopathies.
KW - Alzheimer's disease
KW - retina
KW - tauopathy
KW - vision impairment
UR - http://www.scopus.com/inward/record.url?scp=85168659557&partnerID=8YFLogxK
U2 - https://doi.org/10.1002/alz.13424
DO - https://doi.org/10.1002/alz.13424
M3 - Article
C2 - 37615275
SN - 1552-5260
VL - 20
SP - 330
EP - 340
JO - Alzheimer's and Dementia
JF - Alzheimer's and Dementia
IS - 1
ER -