The review I shared contains many ideas along these lines. Basically the AA sequences seem to be selected to disfavor aggregation, so most mutations should increase formation:
>"Many of the characteristics of proteins that enable the
avoidance of aggregation, and amyloid formation in particular,
are encoded by their amino acid sequences116. The
elucidation of this code has enabled the identification of
factors that determine the intrinsic aggregation propensity
of these molecules117–119. Hence, it has been realized
that globular proteins fold into structures that sequester
aggregation-prone regions in their interior; in addition,
typical features of the folding process, such as very high
cooperativity, generate considerable kinetic barriers to the
conversion of folded proteins into aggregation-prone species50,120.
Furthermore, specific patterns of residues, such
as alternating hydrophobic–hydrophilic stretches50,121, that
tend to favour the amyloid state are commonly selected
against during evolution119,121,122 or are otherwise neutralized
by the insertion of highly aggregation-resistant
residues, which are known as ‘gatekeepers’
(REFS 50,123)."
Really I doubt in the end there will be any disease not associated with amyloid/aggregate formation.
