Table 5.

The effects of sulforaphane on Alzheimer’s disease (AD)-associated biomarkers of synaptic damage and neurodegeneration such as cell death in AD-like models.

Model	Sulforaphane Dose	Findings	Ref.
3×Tg-AD mice	10 or 50 mg/kg p.o., 6 days/week for 2 months	in the frontal cortex: (1) increased MAP2, synaptophysin, and PSD-95 (2) activated TrkB signaling pathway in the cortex and hippocampal CA1: (1) increased BDNF levels	[33]
murine cortical neurons treated with Aβ42	0.01, 0.03 or 0.1 μM pre-treatment for 30 min followed by Aβ42	(1) protected against cell death (2) rescued dendritic integrity	[32]
human neuroblastoma SH-SY5Y cells treated with Aβ25–35	2 μM pre-treatment for 3 h followed by Aβ25–35	(1) protected against cell death (2) up-regulated p75 NTR (3) increased levels of Ace-H3K9 and Ace-H4K12 (4) reduced expression of HDAC1 and 3 suggested to contribute to up-regulation of p75 NTR	[35]
	1–5 μM pre-treatment for 30 min followed by Aβ25–35	(1) protected against cell death (2) reduced Bax/Bcl-2 (3) reduced activation of JNK	[40]
	1 μM co-treatment with Aβ25–35	(1) protected against cell death (2) increased HSP70	[43]
murine neuroblastoma N2A cells treated with Aβ1–42	2.5 μM pre-treatment for 18 h followed by Aβ1–42	(1) protected against cell death (2) sulforaphane effect dependent on proteasome activity	[41]
murine neuroblastoma N1E-115 treated with Aβ1–42	5 μM pre-treatment for 18 h followed by Aβ1–42	(1) protected against cell death

p.o., per os (by mouth).