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Brain Sci. 2018, 8(9), 175; https://doi.org/10.3390/brainsci8090175

The Loss of α- and β-Tubulin Proteins Are a Pathological Hallmark of Chronic Alcohol Consumption and Natural Brain Ageing

1
School of Medicine, University of Nottingham, Royal Derby Hospital Centre, Derby DE22 3DT, UK
2
School of Medicine, Addis Ababa University, Addis Ababa 1000, Ethiopia
3
École nationale supérieure de chimie de Montpellier, 34090 Montpellier, France
4
Department of Experimental Pharmacology and Toxicology, University of Port Harcourt, Port Harcourt 500262, Rivers State, Nigeria
5
Department of Pharmacology, University of the Basque Country, Leioa-Erandio 48940, Spain
6
Centro de Investigación Biomédica en Red de Salud Mental, Madrid 28029, Spain
7
Section of Forensic Pathology, Basque Institute of Legal Medicine, Bilbao 48001, Spain
8
Research Service, Veterans Affairs Nebraska-Western Iowa Health Care System, Omaha, NE 68105, USA
9
Departments of Internal Medicine and Biochemistry & Molecular Biology, University of Nebraska Medical Center, Omaha, NE 68105, USA
These authors contributed equally to this work.
*
Author to whom correspondence should be addressed.
Received: 6 July 2018 / Revised: 19 August 2018 / Accepted: 2 September 2018 / Published: 11 September 2018
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Abstract

Repetitive excessive alcohol intoxication leads to neuronal damage and brain shrinkage. We examined cytoskeletal protein expression in human post-mortem tissue from Brodmann’s area 9 of the prefrontal cortex (PFC). Brain samples from 44 individuals were divided into equal groups of 11 control, 11 alcoholic, 11 non-alcoholic suicides, and 11 suicide alcoholics matched for age, sex, and post-mortem delay. Tissue from alcoholic cohorts displayed significantly reduced expression of α- and β-tubulins, and increased levels of acetylated α-tubulin. Protein levels of histone deacetylase-6 (HDAC6), and the microtubule-associated proteins MAP-2 and MAP-tau were reduced in alcoholic cohorts, although for MAPs this was not significant. Tubulin gene expressions increased in alcoholic cohorts but not significantly. Brains from rats administered alcohol for 4 weeks also displayed significantly reduced tubulin protein levels and increased α-tubulin acetylation. PFC tissue from control subjects had reduced tubulin protein expression that was most notable from the sixth to the eighth decade of life. Collectively, loss of neuronal tubulin proteins are a hallmark of both chronic alcohol consumption and natural brain ageing. The reduction of cytosolic tubulin proteins could contribute to the brain volumetric losses reported for alcoholic patients and the elderly. View Full-Text
Keywords: acetylation; ageing; alcoholism; alcohol-related brain damage; α-tubulin; β-tubulin; HDAC6; MAP-2; MAP-tau; pre-frontal cortex acetylation; ageing; alcoholism; alcohol-related brain damage; α-tubulin; β-tubulin; HDAC6; MAP-2; MAP-tau; pre-frontal cortex
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Labisso, W.L.; Raulin, A.-C.; Nwidu, L.L.; Kocon, A.; Wayne, D.; Erdozain, A.M.; Morentin, B.; Schwendener, D.; Allen, G.; Enticott, J.; Gerdes, H.K.; Johnson, L.; Grzeskowiak, J.; Drizou, F.; Tarbox, R.; Osna, N.A.; Kharbanda, K.K.; Callado, L.F.; Carter, W.G. The Loss of α- and β-Tubulin Proteins Are a Pathological Hallmark of Chronic Alcohol Consumption and Natural Brain Ageing. Brain Sci. 2018, 8, 175.

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