If your competent? doctor isn't actively researching cognitive impairment fixes; you DON'T have a functioning stroke doctor! Don't know what it is, but it's NOT a doctor! Proof that you don't have a doctor is NO followup with human testing!
Host‐Microbial Cometabolite Ursodeoxycholic Acid Protects Against Poststroke Cognitive Impairment
Abstract
Background
Poststroke
cognitive impairment (PSCI) is a common residual disability after
stroke, often underestimated and underdiagnosed. We previously found
that ursodeoxycholic acid (UDCA), a host‐microbiota cometabolite,
ameliorates brain damage in stroke mice. Based on these findings, we
aimed to evaluate the predictive value of UDCA for PSCI risk in a
prospective cohort study.
Methods and Results
We
recruited 202 patients with mild acute ischemic stroke and 63 patients
with symptomatic large‐artery atherosclerotic stenosis as the modeling
and external validation cohorts, respectively. Mice were subjected to
transient middle cerebral artery occlusion, and cognitive function was
assessed using the Morris water maze test. Patients with mild acute
ischemic stroke who developed PSCI exhibited significant alterations in
gut microbiota and plasma bile acid profiles during the acute stroke
phase, including a notable reduction in UDCA level. Through feature
selection and machine learning, we constructed a predictive model for
PSCI incorporating plasma UDCA level, the relative abundance of
Clostridia, Bacilli, and Bacteroides, as well as age, educational
level, and the presence of moderate to severe white matter lesions.
This model exhibited robust predictive performance in both internal
(area under the curve, 0.904 [95% CI, 0.808–1.000]) and external (area
under the curve, 0.838 [95% CI, 0.742–0.934]) validations. Animal
studies in mice also showed reduced UDCA levels in plasma and brain
tissue following stroke. UDCA administration improved cognitive function
in stroke mice by reducing hippocampal microglial activation and
neuronal apoptosis.
Conclusions
Our
findings indicate that UDCA has potential as a biomarker for predicting
PSCI risk and plays a neuroprotective role in the progression of PSCI.
This suggests that early identification and intervention targeting UDCA
could represent a promising strategy for the prevention and treatment of
PSCI.
Graphical Abstract
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