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Table 1 The altered brain BA metabolites in neurological diseases

From: Roles of bile acids signaling in neuromodulation under physiological and pathological conditions

Neurological diseases

BA metabolites in brain

HE

Increased brain BA in CSF (GUDCA and GCA) of HE patients, and total BA contents especially TCA and LCA in HE models.

AD

Lower brain TCA, higher primary BA (GCDCA or TMCA) and secondary BA (DCA, LCA, GDCA, GLCA, GUDCA, TDCA or TLCA), increased the ratios of secondary versus primary BA in brain (DCA:CA, TDCA:CA, GDCA:CA, GDCA:DCA, TLCA:CDCA or GLCA:CDCA) in AD patients.

Decreased brain CA, TCA, TMCA, β-MCA, Ω-MCA, or TUDCA in AD APP/PS1 mice model.

PD

Identified affected BA metabolites (increased DCA, MCA and decreased TCA and GCDCA) in CSF of sporadic PD or genetically predisposed (LRRK2) to PD patients.

HD

Decreased brain CYP46A1 expression and reduced the intermediates 24 S-OHC in HD patients or HD mice models.

CTX

Accumulated cholesterol and cholestenol (CDCA precursor).