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.
References:
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.
Bottino C.M.C., Padua, A.C., Smid,
J., Fegyveres, R.A., Novaretti, T., Bahia V.S. (2011).
Differential diagnosis between dementia and psychiatric disorders. Dement
Neuropsychol. 5(4):288-296.
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. )
