Role of tuberin in neuronal degeneration

Samy L. Habib; David Michel; Eliezer Masliah; Bobby Thomas; Han Seok Ko; Ted M. Dawson; Hanna Abboud; Robert A. Clark; Syed Z. Imam

doi:10.1007/s11064-007-9558-8

Role of tuberin in neuronal degeneration

Samy L. Habib, David Michel, Eliezer Masliah, Bobby Thomas, Han Seok Ko, Ted M. Dawson, Hanna Abboud, Robert A. Clark, Syed Z. Imam

Research output: Contribution to journal › Article › peer-review

9 Scopus citations

Abstract

One of the tuberous sclerosis complex (TSC) gene products, tuberin is assumed to be the functional component, being involved in a wide variety of cellular processes. Here, we report for the first time that tuberin dysfunction may represent a mechanism for neuronal damage in Alzheimer's disease (AD), Parkinson's disease with dementia (PD/DLB), and a mouse model of PD. Tuberin was hyperphosphorylated at Thr1462 in post-mortem frontal cortex tissue of both AD and PD/DLB patients and in mice treated with 1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine hydrochloride (MPTP). Both PTEN and Akt phosphoactivation corresponded to the hyperphosphorylation patterns of tuberin suggesting that the PTEN-Akt pathway might be the mechanism of tuberin phosphorylation. Our data provide new information regarding the possible role of tuberin dysfunction in major neurodegenerative disorders, such as AD and PD, whereby inhibition of tuberin function may trigger an onset of neuronal cell death.

Original language	English (US)
Pages (from-to)	1113-1116
Number of pages	4
Journal	Neurochemical Research
Volume	33
Issue number	6
DOIs	https://doi.org/10.1007/s11064-007-9558-8
State	Published - Jun 2008

Keywords

Akt
Alzheimer's disease
Neurodegeneration
Parkinson's disease
Tuberin
Tuberous sclerosis complex

ASJC Scopus subject areas

Biochemistry
Cellular and Molecular Neuroscience

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10.1007/s11064-007-9558-8

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title = "Role of tuberin in neuronal degeneration",

abstract = "One of the tuberous sclerosis complex (TSC) gene products, tuberin is assumed to be the functional component, being involved in a wide variety of cellular processes. Here, we report for the first time that tuberin dysfunction may represent a mechanism for neuronal damage in Alzheimer's disease (AD), Parkinson's disease with dementia (PD/DLB), and a mouse model of PD. Tuberin was hyperphosphorylated at Thr1462 in post-mortem frontal cortex tissue of both AD and PD/DLB patients and in mice treated with 1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine hydrochloride (MPTP). Both PTEN and Akt phosphoactivation corresponded to the hyperphosphorylation patterns of tuberin suggesting that the PTEN-Akt pathway might be the mechanism of tuberin phosphorylation. Our data provide new information regarding the possible role of tuberin dysfunction in major neurodegenerative disorders, such as AD and PD, whereby inhibition of tuberin function may trigger an onset of neuronal cell death.",

keywords = "Akt, Alzheimer's disease, Neurodegeneration, Parkinson's disease, Tuberin, Tuberous sclerosis complex",

author = "Habib, {Samy L.} and David Michel and Eliezer Masliah and Bobby Thomas and Ko, {Han Seok} and Dawson, {Ted M.} and Hanna Abboud and Clark, {Robert A.} and Imam, {Syed Z.}",

note = "Funding Information: Acknowledgments This work was supported in part by NIH grants NS38377 and NS48206 and grants from American Diabetes Association (ADA), U.S. Dept of Veterans Affairs (VA), American Parkinson{\textquoteright}s Disease Association (APDA), Parkinson{\textquoteright}s Disease Foundation (PDF), San Antonio Area Foundation (SAAF), and Executive Research Council (ERC) of UTHSCSA. T.M.D. is the Leonard and Madlyn Abramson Professor in Neurodegenerative Diseases.",

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doi = "10.1007/s11064-007-9558-8",

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AU - Habib, Samy L.

AU - Michel, David

AU - Masliah, Eliezer

AU - Thomas, Bobby

AU - Ko, Han Seok

AU - Dawson, Ted M.

AU - Abboud, Hanna

AU - Clark, Robert A.

AU - Imam, Syed Z.

N1 - Funding Information: Acknowledgments This work was supported in part by NIH grants NS38377 and NS48206 and grants from American Diabetes Association (ADA), U.S. Dept of Veterans Affairs (VA), American Parkinson’s Disease Association (APDA), Parkinson’s Disease Foundation (PDF), San Antonio Area Foundation (SAAF), and Executive Research Council (ERC) of UTHSCSA. T.M.D. is the Leonard and Madlyn Abramson Professor in Neurodegenerative Diseases.

PY - 2008/6

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N2 - One of the tuberous sclerosis complex (TSC) gene products, tuberin is assumed to be the functional component, being involved in a wide variety of cellular processes. Here, we report for the first time that tuberin dysfunction may represent a mechanism for neuronal damage in Alzheimer's disease (AD), Parkinson's disease with dementia (PD/DLB), and a mouse model of PD. Tuberin was hyperphosphorylated at Thr1462 in post-mortem frontal cortex tissue of both AD and PD/DLB patients and in mice treated with 1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine hydrochloride (MPTP). Both PTEN and Akt phosphoactivation corresponded to the hyperphosphorylation patterns of tuberin suggesting that the PTEN-Akt pathway might be the mechanism of tuberin phosphorylation. Our data provide new information regarding the possible role of tuberin dysfunction in major neurodegenerative disorders, such as AD and PD, whereby inhibition of tuberin function may trigger an onset of neuronal cell death.

AB - One of the tuberous sclerosis complex (TSC) gene products, tuberin is assumed to be the functional component, being involved in a wide variety of cellular processes. Here, we report for the first time that tuberin dysfunction may represent a mechanism for neuronal damage in Alzheimer's disease (AD), Parkinson's disease with dementia (PD/DLB), and a mouse model of PD. Tuberin was hyperphosphorylated at Thr1462 in post-mortem frontal cortex tissue of both AD and PD/DLB patients and in mice treated with 1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine hydrochloride (MPTP). Both PTEN and Akt phosphoactivation corresponded to the hyperphosphorylation patterns of tuberin suggesting that the PTEN-Akt pathway might be the mechanism of tuberin phosphorylation. Our data provide new information regarding the possible role of tuberin dysfunction in major neurodegenerative disorders, such as AD and PD, whereby inhibition of tuberin function may trigger an onset of neuronal cell death.

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Role of tuberin in neuronal degeneration

Abstract

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