Being a cognitive disorder involving the degeneration of brain, progressive loss of memory and lowered life expectancy, Alzheimer’s disease resembles in strange ways to the after effects of alcohol consumption. Obviously both of them serve as a burden to the health, society and economic stability of any nation. Studies on alcohol consumption and tobacco smoking have shown cognitive impairment which is parallel to the usual symptoms of Alzheimer’s. Irrespective of nutritional deficits, progressive psychological decline is observed in chronic alcoholics. Hypothalamus, Cerebellum and the frontal superior cortex are the most predominantly affected areas by the toxic effects of alcohol. In addition they cause significant structural changes in myelin which could be reversible during abstinence.
Alcohol consumption could be attributed as one of the risk factors for developing Alzheimer’s disease, as both of them share biological complications, related with brain chemistry and associated disorders. The main challenge while researching on the impact of alcohol usage on developing Alzheimer’s disease is in diagnosing and distinguishing alcoholic dementia from Alzheimer’s disease.
Heavy alcohol drinking causes both immediate and long term detrimental effects on brain such as accelerating brain shrinkage, eventually leading to neurodegenerative changes and cognitive decline. Comparative investigations by Jensen & Pakkenberg (1993), on subjects with cerebral atrophy caused by aging and alcohol consumption have revealed that, alcohol induced damages are mostly reversible, as it doesn’t cause any change in the number of nerve cells, although considerable death of brain cells, which supports the neurons is observed. Since the brain cells could be regenerated during the process of abstinence, cognitive performance could be improved. While research by Krill & Halliday (1999), have revealed loss of cholinergic neurons that are associated with the chemical messenger of our brain, the neurotransmitter acetyl choline. As any defects in the cholinergic system such as reduction in acetyl choline or reduced protein receptors is well established with the Alzheimer’s disease, chronic alcohol usage could definitely be linked as a cause for Alzheimer’s disease. Shockingly, studies by Arendt (1993) have shown partial reversal of these damages on cholinergic systems upon stimulation by compounds such as nicotine during tobacco smoking, which discloses the controversial hypothesis of decreased association of Alzheimer’s disease with drinkers who smoke.
Speaking of alcohol induced nutritional deficiency; the most frequent one is the vitamin B1 deficiency, which eventually induces Wernicke-Korsakoff syndrome. This syndrome involves isolated or associated symptoms such as mental confusion, abnormal ocular movement and gait ataxia. If left undiagnosed, the patients could either evolve into a serious condition called the Korsakoff’s syndrome or even death. Clinical features and findings on structural neuroimaging of Korsakoff’s syndrome involve episodic memory deficit, variable compromise in semantic memory, nystagmus, cortical atrophy, reduced volume of thalamus and mammillary bodies. Marchiafava-Bignami is a rare disease generally diagnosed in chronic alcoholics with symptoms involving dementia, muscular hypertonia, epileptic episodes, dysphagia etc. This disease has a high lethality rate with most of the patients evolving into a comatose state. Its neuroimaging findings have revealed prominent atrophy of corpus collosum, with varying degrees of necrosis and cystic fibrosis. Alcoholic dementia is yet not uniformly diagnosed during epidemiological studies making the discriminations between alcoholic dementia and Alzheimer’s disease more problematic.
Further clarity is needed to prove the association of alcohol with Alzheimer’s disease. Longitudinal researches are needed which avoids methodological limitations such as the confirmation of investigations on subjects by studying the brain after death. Association of factors ranging from genetic, vascular and even gender should be extensively and thoroughly investigated to clarify the association of alcohol with Alzheimer’s disease.
Arendt, T. (1993). The cholinergic deafferentation of the cerebral cortex induced by chronic consumption of alcohol: Reversal by cholinergic drugs and trans-plantation. In: Hunt, W.A., and Nixon, S.J., eds. Alcohol-Induced Brain Damage. Rockville, MD: U.S. Department of Health and Human Services. 431–460.
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Jensen, G.B., & Pakkenberg, B. (1993). Do alcoholics drink their neurons away? The Lancet. 342:1201– 1204.
Krill, J.J. & Halliday, G.M. (1999). Brain shrinkage in alcoholics: A decade on and what have we learned? Progress in Neurobiology 58:381–387.
Tyas, S.L. (2001). Alcohol use and the risk of developing Alzheimer’s disease. Alcohol Research & Health. Vol: 25, No: 4.
(Review of the original article by Suzanne L. Tyas. Original publication is available from National Institute of Alcohol Abuse and Alcoholism. )