Role of Tuberin in Neuronal Degeneration |
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| Authors: | Samy L Habib David Michel Eliezer Masliah Bobby Thomas Han Seok Ko Ted M Dawson Hanna Abboud Robert A Clark Syed Z Imam |
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| Institution: | (1) Department of Medicine, University of Texas Health Science Center, San Antonio, TX, USA;(2) Departments of Medicine & Pharmacology, University of Texas Health Science Center, San Antonio, TX, USA;(3) Departments of Neurosciences and Pathology, University of California, San Diego, CA, USA;(4) Departments of Neurology and Neurosciences, Institute for Cell Engineering, Johns Hopkins School of Medicine, Baltimore, MD, USA;(5) South Texas Veterans Healthcare System, San Antonio, TX, USA;(6) Present address: Department of Neurology and Neuroscience, Weill Medical College of Cornell University, 525 East 68th Street, A-501, New York, NY 10021, USA |
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| 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. |
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| Keywords: | Tuberous sclerosis complex Parkinson's disease Alzheimer's disease Tuberin Akt Neurodegeneration |
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