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http://dx.doi.org/10.3324/haematol.2015.135459 | DOI Listing |
Alzheimers Dement
December 2024
Edith Cowan University, Perth, Western Australia, Australia.
Background: Accumulation of amyloid beta 42 (Aβ42) senile plaques is the most critical event leading to Alzheimer's disease (AD). Currently approved drugs for AD have not been able to effectively modify the disease. This has caused increasing research interests in health beneficial nutritious plant foods as viable alternative therapy to prevent or manage AD.
View Article and Find Full Text PDFBackground: Although investment in biomedical and pharmaceutical research has increased significantly over the past two decades, there are no oral disease-modifying treatments for Alzheimer's disease (AD).
Method: We performed comprehensive human genetic and multi-omics data analyses to test likely causal relationship between EPHX2 (encoding soluble epoxide hydrolase [sEH]) and risk of AD. Next, we tested the effect of the oral administration of EC5026 (a first-in-class, picomolar sEH inhibitor) in a transgenic mouse model of AD-5xFAD and mechanistic pathways of EC5026 in patient induced Pluripotent Stem Cells (iPSC) derived neurons.
Alzheimers Dement
December 2024
Afe Babalola University, Ado-Ekiti (ABUAD), Ado-Ekiti, Ekiti state, Nigeria.
Background: The impact of probiotics as gut and immunological modulator in restoring gut microbial balance and immune cells expression have generated much attention in the health sector. Its inhibitory effect on bacterial translocation and associated neural inflammatory processes has been reported. However, there is scarcity of data on its neuroprotective impact against neuroinflammation-associated neurodegeneration and memory impairment.
View Article and Find Full Text PDFBackground: TREM2 is a lipid-sensing receptor expressed by microglial sub-populations within neuropathological microenvironments, whose downstream signaling promotes microglial survival, plasticity, and migration. Multiple loss-of-function variants strongly implicate TREM2 as a key regulator of Alzheimer's disease (AD) risk. Accordingly, TREM2 antibodies are currently in development to evaluate the therapeutic potential of TREM2 agonism in neurodegenerative diseases.
View Article and Find Full Text PDFBackground: Seizures in Alzheimer's Disease (AD) are increasingly recognized to occur and can increase cognitive decline and reduce survival compared to unaffected age-matched peers (Lyou et al. 2018). Administration of antiseizure medicines (ASMs) to AD patients with epileptiform activity may improve cognition (Vossel et al.
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