NEFL (Neurofilament Light Chain)

Real-world improvements will depend on standardized diagnostic pathways integrating orbital magnetic resonance imaging (MRI), high-quality antibody assays, OCT, and visual evoked potentials (VEP). Fluid biomarkers such as serum neurofilament light chain (sNfL) and serum glial fibrillary acidic protein (sGFAP), together with AI-supported analytics, may refine risk estimates, especially in seronegative cases.

Successful recanalization with MT is associated with mitigated axonal injury, astrocyte activation, and neuroinflammation, findings consistent with better preservation of NVU integrity. Serum NfL and GFAP represent promising biomarkers for predicting stroke prognosis and tailoring therapeutic strategies.

CTHRC1 overexpression in SH-SY5Y cells promoted tau degradation and modulated network partner expression. CTHRC1 represents a central hub in cognitive function networks, suggesting therapeutic potential for neurodegenerative disorders.

MSA exhibited a significant imbalance in KYN metabolism, suggesting a shift toward inflammatory processes distinct from classic neuroinflammatory markers.

While promising, the translation of these biomarkers into clinical practice is hindered by methodological limitations, including assay heterogeneity and lack of large-scale validation. Future standardization of these molecular signatures is a critical step toward implementing precision medicine in stroke rehabilitation.

The abnormalities detected in SEVs likely reflect oligodendrocyte injury and degeneration, as well as astrocytic activation. The findings suggest that low-invasive SEV approaches, including the novel analysis of ASPH upregulation, can be used to detect and monitor AD white matter degeneration.

Remaining challenges include diagnostic delays, limited high-level evidence, and the paucity of validated biomarkers of disease activity. Future work should prioritize prospective, biomarker-driven trials and multidisciplinary pathways to shorten time to diagnosis and improve long-term outcomes in patients with PNS.

Prospective, mechanism-rich studies-ideally pairing longitudinal stool profiling with inflammatory panels and neuroimaging-are needed before clinical translation. https://www.crd.york.ac.uk/prospero/, identifier CRD42024548645.

Adult patients (>18 years) prescribed at least four cycles of oxaliplatin, cisplatin, docetaxel or paclitaxel were clinically assessed and had blood taken for sNfL analysis at baseline and prior to each cycle. Taxanes cause greater and sharper sNfL rises than platinum agents. Age-adjusted sNfL associates with neuropathy severity in platinum-treated patients; however, in most patients it is unable to detect early axonal damage before this is detectable with clinical examination.

Brain-level disease modification by Kv1.3 blockade was reflected in the cerebrospinal fluid (CSF) via reduced levels of neurofilament-light (NEFL) and resilience protein RPH3A, both of which are increased in human AD CSF. Together, this study demonstrates functional links between Kv1.3 channels and type 2 IFN signaling and reveals distinct cellular effects of Kv1.3 blockers in AD pathology that correspond with reduced neuropathology and neuroinflammation, augmentation of resilience and neuro-vascular pathways, along with biomarkers of therapeutic effect.

Nevertheless, variability in assay performance and sampling timing continues to limit widespread clinical adoption. Future research should prioritize methodological standardization, analytical validation, and the integration of multi-omic data with machine learning-based predictive models.

Biomarkers in FTLD are not only pivotal for diagnosis but also for tracking disease progression and monitoring response to emerging therapies. A comprehensive biomarker panel, incorporating markers of neurodegeneration, neuroinflammation, and specific pathology, may eventually enable personalized treatment approaches as well as evaluate the role of co-pathology.