Clinical MedicineUpdated Aug 18, 2026Version v1
Reviewed milestones, validation shifts, standards, datasets, and debates linked to public evidence.
Evidence from The Lancet Neurology indicates that Significantly higher plasma NfL in HTT mutation carriers vs. controls. This is tracked as a clinical because it changes how Blood Biomarkers for Neurodegeneration is understood, validated, or applied.
Evidence from Alzheimer s & Dementia indicates that AD is redefined as a biological construct based on AT(N) biomarkers. This is tracked as a standard because it changes how Blood Biomarkers for Neurodegeneration is understood, validated, or applied.
Evidence from Alzheimer s & Dementia indicates that Ng and T-tau distinguished Aβ+ from Aβ- individuals in all clinical groups. This is tracked as a clinical because it changes how Blood Biomarkers for Neurodegeneration is understood, validated, or applied.
Evidence from Alzheimer s Research & Therapy indicates that ELISA and SIMOA plasma Aβ 1–42 /Aβ 1–40 ratios demonstrated identical accuracy (AUC 0.78-0.79) in detecting cerebral amyloidosis. This is tracked as a clinical because it changes how Blood Biomarkers for Neurodegeneration is understood, validated, or applied.
Evidence from Molecular Neurodegeneration indicates that CSF biomarkers (Aβ42/40, t-tau, p-tau, NfL) are established diagnostic tools for AD. This is tracked as a standard because it changes how Blood Biomarkers for Neurodegeneration is understood, validated, or applied.
Evidence from Brain indicates that Serum and CSF brain-derived tau were significantly correlated, unlike serum and CSF total-tau. This is tracked as a clinical because it changes how Blood Biomarkers for Neurodegeneration is understood, validated, or applied.
Evidence from Alzheimer s Research & Therapy indicates that Longitudinal GFAP levels increased in retired boxers and were associated with decreasing brain volumes and cognitive decline. This is tracked as a standard because it changes how Blood Biomarkers for Neurodegeneration is understood, validated, or applied.
Evidence from JAMA Neurology indicates that Plasma p-tau217 showed high accuracy in identifying elevated Aβ (AUC, 0.92-0.96) and tau pathology (AUC, 0.93-0.97). This is tracked as a clinical because it changes how Blood Biomarkers for Neurodegeneration is understood, validated, or applied.
Evidence from Molecular Neurodegeneration indicates that Current biomarkers accurately estimate established AD pathologies but miss early stages. This is tracked as a clinical because it changes how Blood Biomarkers for Neurodegeneration is understood, validated, or applied.
Evidence from JAMA Network Open indicates that Nonsmoking group had significantly lower CSF Aβ42 (38.0 pg/mL) and TNFα (23.0 pg/mL) compared to the smoking group (52.8 pg/mL and 28.0 pg/mL, respectively). This is tracked as a commercial because it changes how Blood Biomarkers for Neurodegeneration is understood, validated, or applied.
Evidence from Molecular Neurodegeneration indicates that mTOR is a critical nutrient sensor with homeostatic functions in neurons. This is tracked as a clinical because it changes how Blood Biomarkers for Neurodegeneration is understood, validated, or applied.
Evidence from Alzheimer s & Dementia indicates that BBMs can be used as pre-screeners for AD trials. This is tracked as a standard because it changes how Blood Biomarkers for Neurodegeneration is understood, validated, or applied.