Figure 1.

The disease model deduced from diverse data, as described here. (1) DNA enters the capsid of either a phage (phage T3 is used as an example) or a herpesvirus. Hyper-expansion, with subunit conversion to an α-sheet structure, occurs to accelerate DNA packaging when packaging is slowed (proposed details in [19,32]). (2) In the case of a phage, packaging finishes and a tail is added to the capsid to form a mature phage particle. (3,4) In the case of herpesviruses, amyloid proteins block the progression of the hyper-expanded capsids by converting to an α-sheet structure and then co-assembling with the α-sheet of subunits of the capsid. (5) Alzheimer’s disease is initiated by the over-production of amyloid protein α-sheets, which are toxic. Some amyloid protein α-sheets are subsequently converted to the β-sheet amyloid protein of plaques. However, this conversion is not sufficient to avoid toxicity when Alzheimer’s disease is present (image adapted from [19]).