Skimming a review article on this topic this appears to be the since at least partially discredited amyloid beta Alzheimer's hypothesis, and studies are divided on whether too much or too little copper is a problem.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5810277/
: Scientific evidence has shown that metal ion binding to β-amyloid accelerates amyloid aggregation, which could finally damage the neurons in AD (Pithadia and Lim, 2012). The involvement of copper in AD is controversial, as some studies show copper deficiency in AD, and consequently a need to enhance copper levels (Borchardt et al., 1999; Kessler et al., 2005, 2008a,b; Exley, 2006; Jiao and Yang, 2007; Vural et al., 2010; Kaden et al., 2011; Exley et al., 2012), while other data point to copper overload and therefore a need to reduce copper levels (Cherny et al., 2001; Sparks et al., 2006; Hua et al., 2011; Luo et al., 2011; Ceccom et al., 2012; Eskici and Axelsen, 2012; Brewer, 2014; Squitti et al., 2014b; Yu et al., 2015). An aberrant copper homeostasis with an increase in the labile pool of copper and a decrease in the copper bound to protein is the main up-dated interpretation (Kepp, 2016; Squitti et al., 2016). In this paper, the role of metal ions, particularly copper, in AD is reviewed and discussed.