Trans-Synaptic Spread of Amyloid-β in Alzheimer’s Disease: Paths to β-Amyloidosis

Table 1

Aβ type and aggregation state.

Aβ type/aggregation state	Detection method	References
Aβ oligomers	ELISA	[8, 13–17, 48, 52]; [12, 19, 32]^∗; [18, 38, 40, 41, 47]#; [37]#
	Western blot	[16, 17, 48]; [44]; [46]#; [47]#
Aβ protofibril	Immunoistochemistry	[19]
Aβ plaques	Immunoistochemistry	[12, 19, 44, 45]; [16, 17, 33, 48]; [16, 37, 38, 40–42, 46, 47]#
Amyloid deposition in human brain	Pittsburgh compound B (PIB) PET	[11, 25, 29]; [19–22, 31]

Amyloid-β (Aβ) refers to peptides derived from cleavage of the amyloid precursor protein (APP) by β- and γ-secretase. Soluble Aβ oligomers indicate Aβ species formed by the aggregation of more than one Aβ peptide (monomers). Oligomers are commonly detectable in sample solutions following centrifugation. Aβ protofibrils are aggregates of Aβ oligomers, with lengths of over 40 nm. Aβ fibrils are Aβ aggregates composed predominantly of β-sheet structure and resistant to degradation. These aggregates are often found in proximity of amyloid plaques. Amyloid plaques consist in deposits of insoluble Aβ; indicates studies that report progressive of Aβ accumulation; # indicates studies that demonstrate Aβ spread between distinct brain regions.