Table 1.

Main tau fragments involved in tau pathology

Type of fragments	Associated proteases	Found in CSF	Lesion	References
TauΔD421	Caspase-3, -6, -7	Reported	Axonal loss, mitochondrial dysfunction, tau polymerization, and aggregation in vitro	[116–119]
ΔTau314	Caspase-2	Not yet reported	Mislocalization to dendritic spine, reduction of AMPA receptor, and excitatory neurotransmission	[120, 121]
17 kDa tau	Calpain-1 and -2	Not yet reported	Altering the composition of cytoskeleton, synaptic degeneration through clathrin-mediated pathway, blocking axonal transport	[122, 123]
N224 tau	Calpain-2	Reported	Not clear (but worthy of diagnosis)	[124–126]
Tau1–368	AEP	Reported	Promoting aggregation, promoting the expression of Aβ, phosphorylation inducing memory impairment	[127–130]
Tau168–368	AEP	Not yet reported	Accumulation in microglial cells	[131]
26–230tau (NH2-tau), 26–44 NH2-tau	Caspase and calpain-1 and caplain-2	Reported	Damage of mitochondrial function, presynaptic defect, damage of study/memory function	[110, 132–137]
tau151–391, tau297–391	Unknown	Not yet reported	Form PHFs in vitro and cultured cells	[138, 139]