The idea that clumps of proteins misfolded into stacked beta sheets (beta amyloid plaques, i.e. Alzheimer&#x27;s) tend to cause other proteins to misfold into beta sheets and join the glob. So, exactly like a prion except with a &quot;messier&quot; mechanism that doesn&#x27;t strictly follow A+B-&gt;B+B.<p>Which raises the question: did prion diseases ever really strictly follow A+B-&gt;B+B? Can Alzheimer&#x27;s be transmitted by eating &quot;infected&quot; brain tissue? If the answers are &quot;No&quot; and &quot;Yes&quot;, then it seems that what we mistook for two diseases (because of differing context and symptoms) was actually one underlying mechanism (with different context and symptoms).<p>Disclaimer: I Am Not An Epidemiologist, I am not extensively familiar with recent literature on the subject, I just did a bit of unrelated work in computational protein folding and couldn&#x27;t help but wonder.