Here's the article she shared with her question:
Washington state has the highest mortality rate for Alzheimer’s disease in the U.S., according to data released this week by the National Vital Statistics System.
At 46.3 deaths per 100,000 people, the state’s death rate for the year 2010 far exceeded the national rate of 25.1 deaths per 100,000.
A bit flippantly, I shot off a comment, "It's probably due to coffee." After all, two of the states with the lowest Alzheimer's rates are Utah and Nevada, where there are large numbers of coffee-avoiding LDS people. And everyone knows that Starbucks and rain are the two things that Seattle has in the most abundance.
As I mentioned in another post below, coffee contains salicylates, which are basically really mild aspirin, so it does have a protective effect against regular age-related dementia. But Alzheimer's? That mysterious tau tangle ailment? What's causing that? Look at the countries with the highest Alzheimer's rates. Finland, Italy, Switzerland, other Scandinavian countries, the Netherlands, the USA, Canada, are at the top. Some suggest that it's due to Vitamin D deficiency, but that doesn't really explain things. Minnesota is full of Scandinavian-descent people who don't get enough sunlight during their harsh winter, yet they just have an average (for the USA) Alzheimer's mortality rate there.
Then look at the countries with the highest coffee intake per capita. Finland tops the list again, followed by the Netherlands, Switzerland, and other Scandinavian countries. The USA is a bit lower down on the coffee list, but Washington state alone is probably quite a bit higher than the US average, what with all the coffee bars that manage to turn a profit there.
Maybe it's only coincidence. But I found some hints of what could be a connection between coffee and Alzheimer's. Tau protein tangles appear to be a result of hyperphosphorylation. Chlorogenic acid, apparently consumed mostly via coffee and tea, inhibits DNA methylation by increasing SAH:
The presence of caffeic acid or chlorogenic acid inhibited DNA methylation predominantly through a non-competitive mechanism, and this inhibition was largely due to the increased formation of S-adenosyl--homocysteine (SAH, a potent inhibitor of DNA methylation), resulting from the catechol-O-methyltransferase (COMT)-mediated O-methylation of these dietary catechols.
But we don't want to increase SAH if it decreases the SAM/SAH ratio, for that is associated with hyperphosphorylation of the tau protein and the tangles that correlate with cognitive impairment in Alzheimer's.
J Neurosci. 2012 Jul 4;32(27):9173-81. doi: 10.1523/JNEUROSCI.0125-12.2012.
Acute administration of L-DOPA induces changes in methylation metabolites, reduced protein phosphatase 2Amethylation, and hyperphosphorylation of Tau protein in mouse brain.
Bottiglieri T1, Arning E, Wasek B, Nunbhakdi-Craig V, Sontag JM, Sontag E.
Folate deficiency and hypomethylation have been implicated in a number of age-related neurodegenerative disorders including dementia and Parkinson's disease (PD). Levodopa (L-dopa) therapy in PD patients has been shown to cause an increase in plasma total homocysteine as well as depleting cellular concentrations of the methyl donor, S-adenosylmethionine (SAM), and increasing the demethylated product S-adenosylhomocysteine (SAH). Modulation of the cellular SAM/SAH ratio can influence activity of methyltransferase enzymes, including leucine carboxyl methyltransferase that specifically methylates Ser/Thr protein phosphatase 2A (PP2A), a major Tau phosphatase. Here we show in human SH-SY5Y cells, in dopaminergic neurons, and in wild-type mice that l-dopa results in a reduced SAM/SAH ratio that is associated with hypomethylation of PP2A and increased phosphorylation of Tau (p-Tau) at the Alzheimer's disease-like PHF-1 phospho-epitope. The effect of L-dopa on PP2A and p-Tau was exacerbated in cells exposed to folate deficiency. In the folate-deficient mouse model, L-dopa resulted in a marked depletion of SAM and an increase in SAH in various brain regions with parallel downregulation of PP2A methylation and increased Tauphosphorylation. L-Dopa also enhanced demethylated PP2A amounts in the liver. These findings reveal a novel mechanism involving methylation-dependent pathways in L-dopa induces PP2A hypomethylation and increases Tau phosphorylation, which may be potentially detrimental to neuronal cells.
It's far too little to turn into a publishable hypothesis. Association doesn't equal causation. However, I think it's enough to induce coffee drinkers to consider limiting their intake.