Table 2.

Specific actions of amyloid protein and deposition denoted in research evidence.

Actions	Evidence	Representative reference number
Macroscopic abnormalities	Lardaceous changes in liver, spleen, heart, islets, and kidneys	(3, 51)
Aetiological agent	Alzheimer's disease: amyloid cascade hypothesis	(52)
	Type 2 diabetes	(13, 14)
Product rather than the cause, secondary to other pathogenic events	Alzheimer's disease
	Weak correlation between Aβ deposits and cognitive status	(18, 53, 54)
	Lack of correlation between loss neural function within the regions responsible for memory and the extent of Aβ deposits in that brain region	(55–58)
	Oxidative stress precedes fibrillar depositions of Aβ	(59–61)
	Amyloid fibrils are the product of the innate immune response	(62–64)
	Aβ plaques were identified in cognitively normal elderly people	(65–67)
	Animals with Aβ deposition do not develop clinical signs of the cognitive impairment	(68)
	Treatments targeting on the Aβ plaques have been unsuccessful	(18–22)
Functional amyloid/biological function	Bacterial and mammalian systems
	Curli and aerial hyphae biogenesis	(69–72)
	Silkmoth chorion generation	(73)
	Melanin and other hormones synthesis	(74, 75)
	Epigenetic control of polyamines	(76, 77)
	Haemostatic role	(78)
	Molecular memory	(79, 80)
	Information transfer	(81)
Protective roles	Neuroprotection (Aβ)	(82–85)
	Antioxidant (Aβ and tau)	(86–89)
	Inhibit Aβ toxicity (tau); inhibit prion toxicity	(90, 91)
	Protect against metal-induced toxicity	(92–94)
	Defend against autoimmunity	23 (Aβ42 and Aβ40) 24 (amyloid fibrils) 138 (amyloid fibrils composed of hexameric peptides) 141 (amyloid-forming peptides that exhibited chaperone activity) 139 (mechanism) 140 (mechanism) (51)
	Anti-microbial (Aβ, IAPP and a-synuclein)	147 (Aβ) 150 (Aβ and aggregated Aβ) 151 (IAPP) 152 (α-Syn)