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Cuts to research funding don't just slow science, they dismantle the foundation of future medicine, technology, and public safety. The breakthroughs we'll need in five, ten, or twenty years from now are being built today. When we strip away support, we're trading away our future.
$1021.11
Raised
6
States Involved
35
Advocates
Our Initiatives
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Funding Clinical Trials
Funding Clinical trials is one of our many goals. The project seeks to raise money and donate the funds to the clinical trials of a new immunotherapy for Ewing's Sarcoma, a rare cancer in children, where the funds will help pay for the manufacturing of doses and laboratory expenses.
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Raising Awareness
Lack of knowledge and unreliable sources fuel misinformation in the public. The BioAdvocacy Project aims to educate the world about healthier living practices to stay safe and informed.
How We Operate
1.
The BioAdvocacy Project accepts donations.
2.
Proceedings are donated to clinical trials.
3.
Drug doses & lab expenses are financed.
Our Publications
Alzheimer’s disease (AD) is a neurodegenerative disease characterized by progressive cognitive decline and loss of neuronal integrity. Emerging evidence suggests that RhoA, Rho-associated coiled-coil kinase (ROCK), and their downstream effector molecule glycogen synthase 3β (GSK3β) interact within a complex signaling pathway (RhoA/ROCK/GSK3β) that plays a crucial role in the pathogenesis of AD. RhoA, a small GTPase, along with its downstream effector, ROCK, regulates various cellular processes, including actin cytoskeleton dynamics, apoptosis, and synaptic plasticity. GSK3β, a serine/threonine kinase, plays a key role in neuronal function and AD pathology, including the regulation of tau phosphorylation and amyloid-beta cleavage. Overactive GSK3β has been closely linked to tau hyperphosphorylation, neurodegeneration, and the progression of AD. Thus, GSK3β has been considered as a promising therapeutic target for treating AD and mitigating cognitive impairment. However, clinical trials of GSK3β in AD have faced considerable challenges due to the complexity of the specific neuronal inhibition of GSK3β. In this review, we summarize the literature regarding the relationship of RhoA/ROCK and GSK3β signaling pathways in AD pathogenesis. We further discuss recent findings of the sTREM2-transgelin-2 (TG2) axis as a potential mediator of this complex pathway and provide our review on a novel targeting strategy for AD.
Triggering receptor expressed on myeloid cells 2 (TREM2) is a cell surface receptor belonging to the TREM family that is predominantly expressed on myeloid cells such as granulocytes, monocytes, osteocytes, macrophages, and microglia. Although much of the functionality of TREM2 is not well understood at the molecular level, it is well established that TREM2 plays a significant role in the regulation of a broad definition of macrophage inflammatory responses. Dysregulation of TREM2 has been implicated in a large number of diseases including Alzheimer's disease, Nasu-Hakola disease, bone-related diseases, and atherosclerosis. The TREM2 gene is highly conserved evolutionarily and at the level of controlling its expression. The function of TREM2 is highly conserved across the broad definition of macrophages, including microglia, osteoclasts, and vascular macrophages. This genetic and physiological "niche conservatism" strongly suggests its pivotal role in regulating inflammatory responses. This mini-review summarizes our current understanding of the structure, expression, and function of TREM2 in the pathogenesis of macrophage-mediated diseases.
Prion diseases are neurodegenerative disorders caused by misfolded prion proteins. Although rare, the said diseases are always fatal; they commonly cause death within months of developing clinical symptoms, and their diagnosis is exceptionally difficult pre-mortem. There are no known cures or treatments other than symptomatic care. Given the aggressiveness of prion diseases on onset, therapies after disease onset could be challenging. Prevention to reduce the incidence or to delay the disease onset has been suggested to be a more feasible approach. In this perspective article, we summarize our current understandings of the origin, risk factors, and clinical manifestations of prion diseases. We propose a PCR testing of the blood to identify PRNP gene polymorphisms at codons 129 and 127 in individuals with familial PRNP mutations to assess the risk. We further present the CRISPR/Cas9 gene editing strategy as a perspective preventative approach for these high-risk individuals to induce a polymorphic change at codon 127 of the PRNP gene, granting immunity to prion diseases in selected high-risk individuals, in particular, in individuals with familial PRNP mutations.
Sponsors
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