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LncRNAs regulate gene expression, thus having the possibility to modulate disease progression.
Targeted therapies are used to modulate disease progression by inhibiting a specific protein within a dysregulated signaling pathway [ 2].
From these results, we hypothesized that a key molecule involved in AD pathogenesis is modified with this sugar chain to modulate disease progression.
In order to determine the possible clinical relevance of such LF-treated DC for inducing antigen-specific tolerance or hyporesponsiveness, we assessed their ability to modulate disease progression in the murine CIA, as an experimental model of RA.
Besides differences in size, post-translational modifications of Aβ – including oxidation, phosphorylation, nitration, racemization, isomerization, pyroglutamylation, and glycosylation – generate a plethora of peptides with different physiological and pathological properties that may modulate disease progression.
For example, human bone marrow-derived MSCs (hBM-MSCs) improved functional recovery in both chronic and relapsing-remitting models of mouse EAE, traced their migration into the injured CNS, and assayed their ability to modulate disease progression and the host immune response [ 9].
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This correlation is not absolute, suggesting the existence of yet unknown factors modulating disease progression.
It is now widely recognised that neuroinflammation is a prominent feature of AD brain, with inflammatory responses playing a significant role in modulating disease progression.
Rarely, patients with two SMN2 copies show mild phenotypes (9), suggesting the influence of yet unidentified modifying factors modulating disease progression.
Treatment of TNF-driven Tg197 transgenic mice with PIP-18 significantly modulates disease progression by suppressing arthritis indicators (synovitis, cartilage and bone erosion) as well as circulatory levels of murine sPLA2, IL-6, and human TNF-α.
From a distance, the interaction between disease and depressive disorders confers no pattern of protection or susceptibility in terms of sex steroids; rather, the unique properties of the disease states in conjunction with sex steroids interact to modulate disease symptomology, progression, and mortality.
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