Extensive OC labeling was observed in the hippocampus (A), subiculum (B) and frontal cortex (C) in Alzheimer disease.  A higher magnification photograph illustrates that OC positive deposits were dense and consisted of fine fibrillar material (D). Picture courtesy of Kayed et al., (2007) Biomed Central: Molecular Neurodegeneration, 2: 18.

Amyloid monomeric proteins can sometimes oligomerize into destructive amyloid fibrils.  Amyloidogenic conformations of non-disease related proteins can be created by partial protein misfolding or denaturation. Many degenerative diseases are known to be related to the accumulation of misfolded proteins as amyloid
fibres. These include the amyloid-β peptide plaques and tau neurofibrillary tangles in senile plaques of Alzheimer’s symptomology, the deposition of α-synuclein in the Lewy bodies of Parkinson’s disease, and accumulation of polyglutamine-containing aggregates in Huntington’s disease.