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Carbon monoxide and anti-amyloid-β combination therapy modulates miR-381 and molecular biomarkers in an aluminum chloride-induced rat model of Alzheimer's disease.
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Algaidi Sami Awda
Аннотация
BACKGROUND: Alzheimer's disease (AD) involves intersecting amyloid, tau, oxidative stress, and apoptotic pathways.
OBJECTIVE: To determine whether combining controlled carbon monoxide (CO) exposure with anti-amyloid-β (Aβ) immunotherapy confers additive benefits on AD-relevant molecular and histological readouts in adult male Sprague-Dawley rats.
METHODS: Adult male Sprague-Dawley rats were assigned to one of five groups: Control, AD, CO, anti-Aβ, and a combination group (CO plus anti-Aβ), after induction of AD-like pathology with aluminum chloride (AlCl3). Outcomes included hippocampal Aβ, phosphorylated tau (p-tau), acetylcholinesterase (AChE), NRF2, and p53 (ELISA); hippocampal miR-381 expression (qRT-PCR); and hippocampal/cortical histology. Data were analyzed at the animal level using one-way ANOVA with post hoc tests.
RESULTS: CO and anti-Aβ monotherapies each reduced Aβ burden and tau phosphorylation versus the AD group. The combination produced the most significant shifts toward Control across Aβ, p-tau, AChE, NRF2, and p53, accompanied by significant upregulation of miR-381 and improved histopathology.
CONCLUSIONS: CO-mediated epigenetic/redox modulation and antibody-driven Aβ clearance act in complementary ways to mitigate AD-like pathology. These findings support epigenetic-immunologic combination strategies as a promising direction for preclinical AD therapy.
OBJECTIVE: To determine whether combining controlled carbon monoxide (CO) exposure with anti-amyloid-β (Aβ) immunotherapy confers additive benefits on AD-relevant molecular and histological readouts in adult male Sprague-Dawley rats.
METHODS: Adult male Sprague-Dawley rats were assigned to one of five groups: Control, AD, CO, anti-Aβ, and a combination group (CO plus anti-Aβ), after induction of AD-like pathology with aluminum chloride (AlCl3). Outcomes included hippocampal Aβ, phosphorylated tau (p-tau), acetylcholinesterase (AChE), NRF2, and p53 (ELISA); hippocampal miR-381 expression (qRT-PCR); and hippocampal/cortical histology. Data were analyzed at the animal level using one-way ANOVA with post hoc tests.
RESULTS: CO and anti-Aβ monotherapies each reduced Aβ burden and tau phosphorylation versus the AD group. The combination produced the most significant shifts toward Control across Aβ, p-tau, AChE, NRF2, and p53, accompanied by significant upregulation of miR-381 and improved histopathology.
CONCLUSIONS: CO-mediated epigenetic/redox modulation and antibody-driven Aβ clearance act in complementary ways to mitigate AD-like pathology. These findings support epigenetic-immunologic combination strategies as a promising direction for preclinical AD therapy.