While casually browsing for updates on Alzheimer’s Disease (AD), apolipoprotein E4 (ApoE4) genotype and amyloid beta (Aβ) burden, one title strongly caught the attention of the author of this blog:
Beer Drinking Associates with Lower Burden of Amyloid Beta Aggregation in the Brain: Helsinki Sudden Death Series.
Beer drinking against dementia? This study, published by Kok and colleagues (1) in Alcoholism: Clinical & Experimental Research, at least deserved reading! The authors investigate in this paper the association between the consumption of different alcoholic beverages (spirits, wine, beer) and Aβ aggregation in the brain. Their results rather surprising: beer drinking decreased the prevalence of Aβ-immunoreactivity in brain sections of autopsy cases investigated.
Before looking into details of the study, first a brief background on Aβ and AD. Amyloid plaques or senile plaques are extracellular deposits of the Aβ peptide and are one of the microscopically hallmarks of AD. The Aβ peptide is derived by sequential proteolytic cleavage of the β-amyloid precursor protein (APP) and plaques seem to spread hierarchically throughout the brain in patients with AD (figure 1). AD is a complex disease and little is known about its pathophysiology and cause. Also studies have shown a substantial genetic component in AD, the pattern of inheritance seems far more complex in which genetic risk factors such as ApoE4 work together with environmental factors and life exposure (i.e. life style).
Figure 1: Characteristic progression of Aβ deposition. Senile plaques (left) seem to spread hierarchically throughout the brain in patients with AD (right). Modified from Jucker et al(2)
Kok et al (1) investigated on how alcohol consumption may influence Aβ burden and analysed for this brain sections (frontal cortex) of 125 cases that were known to consume alcohol and of which Aβ data was available. Only beer drinking was negatively associated with the presence of Aβ-immunoreactivity (figure 2); spirits and wine did not show any correlation, and age, as well as ApoE4 genotype were, as expected, strongly associated with Aβ burden.
Figure 2: Aβ-immunoreactivity prevalence in beer drinkers versus non-beer drinkers (unadjusted analyses, n= 125).
The mechanism on how beer consumption may influence Aβ aggregation remains speculative. Regular beer consumers were shown to have increased levels of B vitamins and folate, as well as reduced levels of total homocysteine. High blood levels of homocysteine (hyperhomocysteinemia) seem to increase the risk for endothelial cell injury that may result in stroke and are associated with a wide range of diseases including thrombosis and AD (for review see (3)). However, how this links to Aβ burden clearly needs further investigation. Nevertheless, the study by Kok et al (1) is unique and is the first study that assesses the effects of alcohol consumption on post-mortem Aβ aggregation.
The author of this blog wants to emphasize that after reading this blog it is not advisable to drink more beer now. As most are surely aware, excessive use of alcohol can lead to cognitive impairment and many other undesirable things.
Blog written by: Lucas Kraft
- Kok, E. H., Karppinen, T. T., Luoto, T., Alafuzoff, I., and Karhunen, P. J. (2016) Beer Drinking Associates with Lower Burden of Amyloid Beta Aggregation in the Brain: Helsinki Sudden Death Series. Alcohol. Clin. Exp. Res. 10.1111/acer.13102
- Jucker, M., and Walker, L. C. (2013) Self-propagation of pathogenic protein aggregates in neurodegenerative diseases. Nature. 501, 45–51
- Morris, M. S. (2003) Homocysteine and Alzheimer’s disease. Lancet. Neurol. 2, 425–8