Exact(7)
Numerous examples exist of species that persist under conditions that promote pathology in humans and considerable insight has been garnered by uncovering the molecular mechanisms mediating this "evolutionary experimentation".
These observations support the view that it is during puberty and early adulthood that testicular androgens induce developmental changes that promote pathology in later life [ 15].
Further catalysis by sPLA2 through surface interactions can then initiate and promote pathology by releasing AA, which can subsequently be converted to proinflammatory prostaglandins and leukotrienes.
Mitochondrial dysfunction may promote pathology during both acute inflammatory events as well as during the progression of neurodegeneration (Su et al., 2013).
Recent studies have established that iron deposition begins early in the disease course (Al-Radaideh et al., 2013) and can promote pathology, e.g., oxidative damage and enhanced production of pro-inflammatory cytokines (Mehta et al., 2013; Hametner et al., 2013).
Recent evidence has suggested that decreased histone deacetylase (HDAC) activity in RA patient synovial tissue may relax the chromatin structure and promote pathology by enhancing transcription of inflammatory gene products [ 8].
Similar(53)
There is also evidence, albeit much more limited, that factors that might protect from Aβ pathology might promote tau pathology and vice versa [ 57- 60].
Both A β and Tau promote cofilin actin pathology, cofilin actin pathology is widespread in AD brains, and cofilin activity is also increased in AD brains.
Correlation is not causality: It may be taken as evidence of Aβ pathology causing or promoting tau pathology, of tau pathology causing or promoting the development of Aβ pathology, or of a third (currently unknown) variable responsible for the synchronous development of the two pathologies.
For example, our data and that from other groups show that an M1-like pro-inflammatory microglial activation state protects from Aβ pathology, whereas an M2-like alternative activation state can promote Aβ pathology [ 41- 49].
Inhibition of RanBP9 and SSH1 may not be sufficient to fully block cofilin actin pathology, as ROS pathways acting directly on cofilin may also promote cofilin actin pathology.
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