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Published on: March 16, 2016
Mildronate improves cognition and reduces amyloid-β pathology in transgenic Alzheimer's disease mice
Ulrika Beitnere1, Thomas van Groen, Ashish Kumar
1Department of Pharmacology, Faculty of Medicine, University of Latvia, Riga, Latvia.
Abstract:
Mildronate, a carnitine congener drug, previously has been shown to provide neuroprotection in an azidothymidine-induced mouse model of neurotoxicity and in a Parkinson's disease rat model. The aim of this study was to investigate the effects of mildronate treatment on cognition and pathology in Alzheimer's disease (AD) model mice (APP(SweDI)). Mildronate was administered i.p. daily at 50 or 100 mg/kg for 28 days. At the end of treatment, the animals were behaviorally and cognitively tested, and brains were assessed for AD-related pathology, inflammation, synaptic markers, and acetylcholinesterase (AChE). The data show that mildronate treatment significantly improved animal performance in water maze and social recognition tests, lowered amyloid-β deposition in the hippocampus, increased expression of the microglia marker Iba-1, and decreased AChE staining, although it did not alter expression of proteins involved in synaptic plasticity (GAP-43, synaptophysin, and GAD67). Taken together, these findings indicate mildronate's ability to improve cognition and reduce amyloid-β pathology in a mouse model of AD and its possible therapeutic utility as a disease-modifying drug in AD patients.
Insights
Mildronate improved cognition and reduced Alzheimer's disease (AD) pathology in mice. This carnitine congener drug shows potential as a disease-modifying therapy for AD patients.
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Mildronate (a carnitine congener) demonstrates neuroprotective effects in various models.
- Alzheimer's disease (AD) is characterized by cognitive decline and specific neuropathologies.
Purpose of the Study:
- To evaluate mildronate's impact on cognition and Alzheimer's disease pathology in a mouse model.
- Investigate mildronate's effects on amyloid-beta deposition, inflammation, and synaptic markers.
Main Methods:
- APP(SweDI) mice received daily intraperitoneal injections of mildronate (50 or 100 mg/kg) for 28 days.
- Cognitive functions were assessed using water maze and social recognition tests.
- Brain tissues were analyzed for AD pathology, inflammation (Iba-1), acetylcholinesterase (AChE), and synaptic markers.
Main Results:
- Mildronate treatment significantly enhanced performance in cognitive tests.
- Reduced amyloid-beta deposition in the hippocampus and decreased AChE staining were observed.
- Increased expression of the microglia marker Iba-1 indicated an anti-inflammatory effect.
Conclusions:
- Mildronate treatment improved cognitive function and ameliorated key Alzheimer's disease pathologies in a mouse model.
- These findings suggest mildronate's potential as a therapeutic agent for Alzheimer's disease.
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