| Amyloid peptides | Aβ42/Aβ40 ratio | Reflects cerebral amyloid plaque burden through changes in the relative concentration of amyloid-β 42 and amyloid-β 40. | Supports assessment of brain amyloid status in people evaluated for cognitive impairment; may help determine eligibility for disease-modifying treatment pathways. | High and established | Directly related to amyloid pathology; minimally invasive; suitable for scalable testing when assays are well validated. | Results can vary by assay platform, pre-analytical handling and population; not a stand-alone diagnosis of dementia. | High-sensitivity immunoassay or targeted mass spectrometry; interpretation should use assay-specific reference limits. |
| Phosphorylated tau | p-tau181 | Indicates tau phosphorylation associated with Alzheimer-type pathology and is often correlated with amyloid and tau abnormalities. | Differential assessment of suspected Alzheimer disease and biological staging in memory-clinic populations. | High; increasingly used clinically | More disease-specific than many general neurodegeneration markers; can rise before advanced clinical decline. | May be influenced by age, kidney function and non-Alzheimer neurodegenerative conditions; thresholds are method-dependent. | Ultra-sensitive immunoassay or mass spectrometry with strict calibration and quality control. |
| Phosphorylated tau | p-tau217 | Reflects Alzheimer-related tau phosphorylation and shows a strong relationship with amyloid and tau pathology. | High-priority blood biomarker for identifying Alzheimer biology and triaging patients for confirmatory evaluation. | Very promising; clinical implementation expanding | Often demonstrates strong diagnostic performance in research cohorts; may reduce reliance on invasive or expensive tests. | Assay standardization, regulatory availability and independent validation across diverse populations remain important considerations. | Ultra-sensitive immunoassay or targeted mass spectrometry; results should not be transferred between platforms without validation. |
| Phosphorylated tau | p-tau231 | Captures an early Alzheimer-associated tau phosphorylation change and may track amyloid-related disease processes. | Early detection research, risk stratification and monitoring of biological change. | Emerging clinical biomarker | Potentially sensitive to early amyloid-related changes, including preclinical disease stages. | Less harmonized clinical evidence than established amyloid measures; interpretation depends strongly on assay performance and study population. | Ultra-sensitive immunoassay or mass spectrometry in specialized laboratories. |
| Neuroaxonal injury | Neurofilament light chain (NfL) | Indicates axonal injury and neuronal damage across several neurological disorders. | General neurodegeneration assessment, disease-progression monitoring and differentiation of low versus high neuronal injury burden. | High for monitoring; limited specificity for Alzheimer disease | Widely applicable; useful for longitudinal monitoring and relatively accessible through blood collection. | Not specific to Alzheimer disease; affected by age, renal function and other neurological or systemic conditions. | Ultra-sensitive immunoassay, usually interpreted with age-adjusted and clinically validated reference ranges. |
| Astrocyte injury or activation | Glial fibrillary acidic protein (GFAP) | Reflects astrocytic activation or injury and is associated with amyloid-related and other neurological processes. | Risk enrichment, early biological screening and complementary interpretation alongside amyloid or phosphorylated tau markers. | Emerging and clinically useful as a complement | May increase early in Alzheimer-related disease and can add context to neuronal-injury markers. | Not disease-specific; affected by age, acute neurological injury and assay differences. | Ultra-sensitive immunoassay with population- and method-specific interpretation. |
| Total tau | Plasma total tau | Represents circulating tau associated with neuronal injury, but does not specify the underlying cause. | Research use and supportive assessment of neuronal injury; generally not preferred as a stand-alone Alzheimer Biomarker. | Established research use; limited routine specificity | Biologically relevant and measurable with sensitive platforms. | Lower disease specificity and weaker clinical discrimination than several phosphorylated tau measures; low circulating concentrations can challenge measurement. | Ultra-sensitive immunoassay or mass spectrometry with careful control of sample handling. |
| Composite biomarker panels | Aβ42/Aβ40 + p-tau + NfL or GFAP | Combines disease-specific amyloid or tau signals with markers of neuronal or glial injury. | Patient triage, diagnostic support, biological staging and research screening when a single marker is insufficient. | Rapidly developing; validation required for each intended use | Can improve robustness by integrating complementary biological processes and may support risk-based workflows. | Higher cost and complexity; algorithm transferability, cutoff selection and clinical validation are essential. | Multiplex immunoassay or separately measured analytes combined through a validated clinical algorithm. |