Table 1 Bile acids and their impact on cognition and dementia
From: Microbial-derived metabolites as a risk factor of age-related cognitive decline and dementia
Bile Acid | In Vitro/ In Vivo (species) | Model | Findings | Reference |
|---|---|---|---|---|
CA (Primary Bile Acid) | In Vivo (Male Sprague-Drawly rats) | Ibotenic Acid-Induced Dementia Model | A combination of administering baicalin, jasminoidin and cholic acid improved cognitive performance through the promotion of pathways related to neuroprotection and neurogenesis | [144] |
In Vivo (Zebrafish) | Zebrafish embryos exposed to a cholic acid-treated medium | Cholic acid was identified as a new Lxr ligand, which in turn promoted neural development and neurogenesis in the midbrain of zebrafish | [137] | |
CDCA (Primary Bile Acid) | In Vivo (Adult male Wistar rats) | AlCl3 induced AD | CDCA treatment reduces neurotoxicity and cognitive decline via increased insulin signalling | [145] |
In Vitro | Primary dissociated cultures of the posterior hypothalamus | CDCA is an antagonist for NMDA and GABAA receptors and can significantly reduce neuronal firing | [146] | |
TCA (Primary Conjugated Bile Acid) | In Vivo (human) | Human brain tissue with AD pathology vs age-matched healthy controls | TCA was significantly lower (p = 0.01) in AD patients than in age-matched controls | [117] |
DCA (Secondary Bile Acid) | In Vitro | BCS-TC2 human colon adenocarcinoma cells | DCA modulates mitochondrial pathways causing apoptosis | [130] |
In Vivo (human) | Serum samples from AD patients, amnesic MCI patients and healthy controls | DCA was increased in amnesic MCI and AD in comparison to healthy controls and correlated with cognitive symptoms | [129] | |
LCA (Secondary Bile Acid) | In Vivo (human) | Plasma samples from patients with AD, MCI and healthy controls | LCA was significantly higher in AD patients (p = 0.004) compared to healthy controls | [147] |
UDCA (Secondary Bile Acid) | In Vitro | BV-2 microglial cell line | UDCA can initiate an anti-inflammatory effect by inhibiting NF-κB activation | [148] |
TUDCA (Secondary Conjugated Bile Acid) | In Vitro | Neuron cell cultures and primary rat neurons | Inhibition of the E2F-1/p53/Bax pathway, leading to suppression of Aβ-induced apoptosis | [138] |
In Vitro | Primary cultures of rat cortical and hippocampal neurons | Reduction in synaptic deficits induced by Aβ through inhibiting the downregulation of postsynaptic density protein-95, leading to a reduction in neuronal death | [149] | |
In Vivo (mouse) | AD model: APP/PS1 double transgenic mice | Dietary TUDCA provided for 6 months decreased Aβ aggregation and enhanced memory retention | [141] | |
In Vivo (mouse) | AD model: APP/PS1 double transgenic mice | Dietary TUDCA provided for 6Â months decreased hippocampal and prefrontal amyloid deposition and inhibited spatial, recognition and contextual memory deficiencies | [150] | |
In Vivo (mouse) | AD model: APP/PS1 double transgenic mice | Intraperitoneal injections of TUDCA decreased Aβ deposition, glycogen synthase kinase 3β activity, phosphorylation of τ, and neuroinflammation | [142] | |
In Vitro | Aβ-treated primary rat cortical neurons | TUDCA prevented Aβ induced cytochrome c release and neuronal death through the PI3K signalling pathway | [151] | |
In Vitro | Aβ-treated primary rat cortical neurons | TUDCA reduced Aβ induced apoptosis through the binding to mineralocorticoid receptors | [140] |