Reducing acetylated tau is neuroprotective in brain injury

Traumatic brain injury (TBI) is the largest non-genetic, non-aging related risk factor for Alzheimer's disease (AD). We report here that TBI induces tau acetylation (ac-tau) at sites acetylated also in human AD brain. This is mediated by S-nitrosylated-GAPDH, which simultaneously inactivates Si...

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Vydáno v:Cell Ročník 184; číslo 10; s. 2715
Hlavní autoři: Shin, Min-Kyoo, Vázquez-Rosa, Edwin, Koh, Yeojung, Dhar, Matasha, Chaubey, Kalyani, Cintrón-Pérez, Coral J, Barker, Sarah, Miller, Emiko, Franke, Kathryn, Noterman, Maria F, Seth, Divya, Allen, Rachael S, Motz, Cara T, Rao, Sriganesh Ramachandra, Skelton, Lara A, Pardue, Machelle T, Fliesler, Steven J, Wang, Chao, Tracy, Tara E, Gan, Li, Liebl, Daniel J, Savarraj, Jude P J, Torres, Glenda L, Ahnstedt, Hilda, McCullough, Louise D, Kitagawa, Ryan S, Choi, H Alex, Zhang, Pengyue, Hou, Yuan, Chiang, Chien-Wei, Li, Lang, Ortiz, Francisco, Kilgore, Jessica A, Williams, Noelle S, Whitehair, Victoria C, Gefen, Tamar, Flanagan, Margaret E, Stamler, Jonathan S, Jain, Mukesh K, Kraus, Allison, Cheng, Feixiong, Reynolds, James D, Pieper, Andrew A
Médium: Journal Article
Jazyk:angličtina
Vydáno: United States 13.05.2021
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ISSN:1097-4172, 1097-4172
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Abstract Traumatic brain injury (TBI) is the largest non-genetic, non-aging related risk factor for Alzheimer's disease (AD). We report here that TBI induces tau acetylation (ac-tau) at sites acetylated also in human AD brain. This is mediated by S-nitrosylated-GAPDH, which simultaneously inactivates Sirtuin1 deacetylase and activates p300/CBP acetyltransferase, increasing neuronal ac-tau. Subsequent tau mislocalization causes neurodegeneration and neurobehavioral impairment, and ac-tau accumulates in the blood. Blocking GAPDH S-nitrosylation, inhibiting p300/CBP, or stimulating Sirtuin1 all protect mice from neurodegeneration, neurobehavioral impairment, and blood and brain accumulation of ac-tau after TBI. Ac-tau is thus a therapeutic target and potential blood biomarker of TBI that may represent pathologic convergence between TBI and AD. Increased ac-tau in human AD brain is further augmented in AD patients with history of TBI, and patients receiving the p300/CBP inhibitors salsalate or diflunisal exhibit decreased incidence of AD and clinically diagnosed TBI.
AbstractList Traumatic brain injury (TBI) is the largest non-genetic, non-aging related risk factor for Alzheimer's disease (AD). We report here that TBI induces tau acetylation (ac-tau) at sites acetylated also in human AD brain. This is mediated by S-nitrosylated-GAPDH, which simultaneously inactivates Sirtuin1 deacetylase and activates p300/CBP acetyltransferase, increasing neuronal ac-tau. Subsequent tau mislocalization causes neurodegeneration and neurobehavioral impairment, and ac-tau accumulates in the blood. Blocking GAPDH S-nitrosylation, inhibiting p300/CBP, or stimulating Sirtuin1 all protect mice from neurodegeneration, neurobehavioral impairment, and blood and brain accumulation of ac-tau after TBI. Ac-tau is thus a therapeutic target and potential blood biomarker of TBI that may represent pathologic convergence between TBI and AD. Increased ac-tau in human AD brain is further augmented in AD patients with history of TBI, and patients receiving the p300/CBP inhibitors salsalate or diflunisal exhibit decreased incidence of AD and clinically diagnosed TBI.Traumatic brain injury (TBI) is the largest non-genetic, non-aging related risk factor for Alzheimer's disease (AD). We report here that TBI induces tau acetylation (ac-tau) at sites acetylated also in human AD brain. This is mediated by S-nitrosylated-GAPDH, which simultaneously inactivates Sirtuin1 deacetylase and activates p300/CBP acetyltransferase, increasing neuronal ac-tau. Subsequent tau mislocalization causes neurodegeneration and neurobehavioral impairment, and ac-tau accumulates in the blood. Blocking GAPDH S-nitrosylation, inhibiting p300/CBP, or stimulating Sirtuin1 all protect mice from neurodegeneration, neurobehavioral impairment, and blood and brain accumulation of ac-tau after TBI. Ac-tau is thus a therapeutic target and potential blood biomarker of TBI that may represent pathologic convergence between TBI and AD. Increased ac-tau in human AD brain is further augmented in AD patients with history of TBI, and patients receiving the p300/CBP inhibitors salsalate or diflunisal exhibit decreased incidence of AD and clinically diagnosed TBI.
Traumatic brain injury (TBI) is the largest non-genetic, non-aging related risk factor for Alzheimer's disease (AD). We report here that TBI induces tau acetylation (ac-tau) at sites acetylated also in human AD brain. This is mediated by S-nitrosylated-GAPDH, which simultaneously inactivates Sirtuin1 deacetylase and activates p300/CBP acetyltransferase, increasing neuronal ac-tau. Subsequent tau mislocalization causes neurodegeneration and neurobehavioral impairment, and ac-tau accumulates in the blood. Blocking GAPDH S-nitrosylation, inhibiting p300/CBP, or stimulating Sirtuin1 all protect mice from neurodegeneration, neurobehavioral impairment, and blood and brain accumulation of ac-tau after TBI. Ac-tau is thus a therapeutic target and potential blood biomarker of TBI that may represent pathologic convergence between TBI and AD. Increased ac-tau in human AD brain is further augmented in AD patients with history of TBI, and patients receiving the p300/CBP inhibitors salsalate or diflunisal exhibit decreased incidence of AD and clinically diagnosed TBI.
Author Chiang, Chien-Wei
Barker, Sarah
Motz, Cara T
Cheng, Feixiong
Gan, Li
Noterman, Maria F
Vázquez-Rosa, Edwin
Rao, Sriganesh Ramachandra
Koh, Yeojung
Kraus, Allison
Jain, Mukesh K
Tracy, Tara E
Chaubey, Kalyani
Fliesler, Steven J
Torres, Glenda L
Savarraj, Jude P J
Franke, Kathryn
Dhar, Matasha
Hou, Yuan
Whitehair, Victoria C
Flanagan, Margaret E
McCullough, Louise D
Shin, Min-Kyoo
Allen, Rachael S
Ahnstedt, Hilda
Kitagawa, Ryan S
Li, Lang
Pardue, Machelle T
Liebl, Daniel J
Choi, H Alex
Pieper, Andrew A
Seth, Divya
Miller, Emiko
Ortiz, Francisco
Williams, Noelle S
Gefen, Tamar
Wang, Chao
Reynolds, James D
Cintrón-Pérez, Coral J
Stamler, Jonathan S
Zhang, Pengyue
Skelton, Lara A
Kilgore, Jessica A
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  givenname: Min-Kyoo
  surname: Shin
  fullname: Shin, Min-Kyoo
  organization: Harrington Discovery Institute, University Hospitals Cleveland Medical Center, Cleveland, OH, USA; Department of Psychiatry, Case Western Reserve University, Cleveland, OH, USA; Geriatric Psychiatry, GRECC, Louis Stokes Cleveland VA Medical Center; Cleveland, OH, USA; Institute for Transformative Molecular Medicine, School of Medicine, Case Western Reserve University, Cleveland, OH, USA
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  organization: Harrington Discovery Institute, University Hospitals Cleveland Medical Center, Cleveland, OH, USA; Department of Psychiatry, Case Western Reserve University, Cleveland, OH, USA; Geriatric Psychiatry, GRECC, Louis Stokes Cleveland VA Medical Center; Cleveland, OH, USA; Institute for Transformative Molecular Medicine, School of Medicine, Case Western Reserve University, Cleveland, OH, USA
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  organization: Harrington Discovery Institute, University Hospitals Cleveland Medical Center, Cleveland, OH, USA; Department of Psychiatry, Case Western Reserve University, Cleveland, OH, USA; Geriatric Psychiatry, GRECC, Louis Stokes Cleveland VA Medical Center; Cleveland, OH, USA; Institute for Transformative Molecular Medicine, School of Medicine, Case Western Reserve University, Cleveland, OH, USA
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  surname: Noterman
  fullname: Noterman, Maria F
  organization: Department of Psychiatry, University of Iowa Carver College of Medicine, Iowa City, IA, USA
– sequence: 11
  givenname: Divya
  surname: Seth
  fullname: Seth, Divya
  organization: Institute for Transformative Molecular Medicine, School of Medicine, Case Western Reserve University, Cleveland, OH, USA; Department of Medicine, University Hospitals Cleveland Medical Center, Cleveland, OH, USA
– sequence: 12
  givenname: Rachael S
  surname: Allen
  fullname: Allen, Rachael S
  organization: Center for Visual and Neurocognitive Rehabilitation, Atlanta VA Healthcare System, Atlanta, GA, USA; Department of Biomedical Engineering, Georgia Institute of Technology, Atlanta, GA, US
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  givenname: Cara T
  surname: Motz
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  organization: Center for Visual and Neurocognitive Rehabilitation, Atlanta VA Healthcare System, Atlanta, GA, USA; Department of Biomedical Engineering, Georgia Institute of Technology, Atlanta, GA, US
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  givenname: Sriganesh Ramachandra
  surname: Rao
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  organization: Departments of Ophthalmology and Biochemistry, and the Neuroscience Graduate Program, SUNY-University at Buffalo, Buffalo, NY, USA; Research Service, VA Western NY Healthcare System, Buffalo, NY, USA
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  surname: Pieper
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  email: andrew.pieper@harringtondiscovery.org
  organization: Harrington Discovery Institute, University Hospitals Cleveland Medical Center, Cleveland, OH, USA; Department of Psychiatry, Case Western Reserve University, Cleveland, OH, USA; Geriatric Psychiatry, GRECC, Louis Stokes Cleveland VA Medical Center; Cleveland, OH, USA; Institute for Transformative Molecular Medicine, School of Medicine, Case Western Reserve University, Cleveland, OH, USA; Weill Cornell Autism Research Program, Weill Cornell Medicine of Cornell University, New York, NY, USA; Department of Neuroscience, Case Western Reserve University, School of Medicine, Cleveland, OH, USA. Electronic address: andrew.pieper@harringtondiscovery.org
BackLink https://www.ncbi.nlm.nih.gov/pubmed/33852912$$D View this record in MEDLINE/PubMed
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Keywords acetylation
congenital muscular dystrophy
omigapil
P7C3
Alzheimer’s disease
salsalate
neuroprotection
diflunisal
neurodegeneration
traumatic brain injury
tau
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PublicationTitle Cell
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References 35590136 - Med. 2021 Jun 11;2(6):637-639
33953376 - Nat Rev Neurosci. 2021 Jun;22(6):325
33888906 - Nat Rev Drug Discov. 2021 Jun;20(6):424
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Snippet Traumatic brain injury (TBI) is the largest non-genetic, non-aging related risk factor for Alzheimer's disease (AD). We report here that TBI induces tau...
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SubjectTerms Acetylation
Alzheimer Disease - etiology
Alzheimer Disease - metabolism
Alzheimer Disease - prevention & control
Animals
Anti-Inflammatory Agents, Non-Steroidal - therapeutic use
Biomarkers - blood
Biomarkers - metabolism
Brain Injuries, Traumatic - complications
Brain Injuries, Traumatic - metabolism
Cell Line
Diflunisal - therapeutic use
Female
Glyceraldehyde-3-Phosphate Dehydrogenase (Phosphorylating)
Humans
Male
Mice
Mice, Inbred C57BL
Neurons - metabolism
Neuroprotection
p300-CBP Transcription Factors - antagonists & inhibitors
p300-CBP Transcription Factors - metabolism
Salicylates - therapeutic use
Sirtuin 1 - metabolism
tau Proteins - blood
tau Proteins - metabolism
Title Reducing acetylated tau is neuroprotective in brain injury
URI https://www.ncbi.nlm.nih.gov/pubmed/33852912
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