Table 1.

TUDCA effects in experimental models of Alzheimer’s diseases

Model /Subject	Effect	Ref.
Mouse neuroblastoma cells	↓ p53 and its downstream targets	[168]
Rat cortical neurons	↓ Translocation of pro-apoptotic Bax to the mitochondria	[173]
Rat neuronal-like PC12 cells	↓ E2F1-p53 apoptotic pathway	[174]
	↓ Caspases activation	[175]
	↓ JNK early activation	[176]
Rat neuronal-like PC12 cells and primary cortical neuron	↓ Anti-apoptotic ΔNp63 degradation	[177]
Human cerebral endothelial cells	↓ Apoptosis induced by the vasculotropic E22Q mutant of Aβ (AβE22Q)	[178]
	↓ Cytochrome c release from mitochondria
	↓ Bax translocation
APOE4 macrophages with ApoE4-induced ER stress	↑ Efferocytosis	[179]
	↓ Cell death
	↓ LPS- and oxidized LDL-induced apoptosis
APP/PS1 mice	↓ mEPSCs	[180]
	↑ Number of dendritic spines
	↑ Postsynaptic marker PSD-95
	↓ Synaptic loss	[181]
	↓ Aβ plaque accumulation	[172, 182]
	↑ Spatial, recognition, and contextual memory
	↓ Activation of astrocytes and microglia	[172]
	↑ Immunoreactivity of MAP2 used as a marker of neuronal integrity
	↓ APOE gene expression	[172]
	↓ Amyloidogenic AβPP processing pathway	[172, 181]
	↓ Aβ41 and Aβ42 levels

ApoE, apolipoprotein E; AβPP, amyloid-β protein precursor; Bax, Bcl-2-associated X protein; ER, endoplasmic reticulum; JNK, c-Jun N-terminal kinase; LPS, lipopolysaccharide; MAP2, microtubule-associated protein 2; mEPSCs, miniature excitatory postsynaptic currents; PS1, presenilin 1; PSD-95, postsynaptic density protein 95.