Table 1.

Biological effects of synthetic, cell-derived, and brain-derived Aβ in different models.

Effect	Source of Aβ	Models
		Cells	In Vivo	Slices
Tau phosphorylation and cytoskeletal disruption	Synthetic Aβ	+ (100–500 nM) [31,33,35]	+ (100 µM, single injection or prolonged infusion) [69,70]	+ (100–500 nM) [97,98,99]
	Cell-derived Aβ	++ (0.2–0.5 nM) [29,34]	nd	nd
	Brain-derived Aβ	++ (0.2–0.5 nM) [33]	++ (nM, single injection) [71]	+/− (1 nM, only in combination with sAβ) [100]
Receptor interaction (NMDAR, AMPAR, nAChR)	Synthetic Aβ	+ (300–500 nM–10 µM) [38,39,40,41,44,45]	+ [72]	+ [91,92]
	Cell-derived Aβ	++ (subnanomolar concentrations) [42,46]	++ (pM) [73]	+ [91,92,101]
	Brain-derived Aβ	nd	+ (transgenic animals) [38,74]	+ [91,92]
Cognitive dysfunction/inhibition of LTP	Synthetic Aβ	n/a	+ (µM) [76,77,80]	+ (200–500 nM) [72,91,92,93,94,95]
	Cell-derived Aβ	n/a	++ (pM) [76,79]	++ (100–300 pM–1 nM) [91,92,93,96]
	Brain-derived Aβ	n/a	+ (micromolar concentrations) [75,76,77,78]	+ [75,91,92]
Physiological role: plasticity, survival	Synthetic Aβ	++ (nM) [48,49,53]	++ (pM) [80,90]	++ (pM) [80,90]
	Cell-derived Aβ	+/− (endogenous only) [48,49]	nd	nd
	Brain-derived Aβ	++ (1 nM) [54]	++ (pM, endogenous) [89]	++ (pM, endogenous) [89]

“+”—the presence of an effect, “++”—the presence of an effect at a physiological concentration of Aβ, “+/−”—controversial data, “nd”—no data: no studies were found, “n/a”—not applicable for this model.