Plasma Biomarkers In Neurodegeneration is an important component in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes.
Plasma biomarkers represent a transformative advancement in the diagnosis and monitoring of neurodegenerative diseases, offering minimally invasive, scalable, and cost-effective alternatives to cerebrospinal fluid (CSF) analysis and neuroimaging. Blood-based biomarkers detect pathological proteins and markers of neuronal injury that leak from the brain into the bloodstream, enabling the identification of conditions such as [Alzheimer's disease[/diseases/[alzheimers[/diseases/[alzheimers[/diseases/[alzheimers--TEMP--/diseases)--FIX--, [Parkinson's disease[/diseases/[parkinsons[/diseases/[parkinsons[/diseases/[parkinsons--TEMP--/diseases)--FIX--, [frontotemporal dementia[/diseases/[ftd[/diseases/[ftd[/diseases/[ftd--TEMP--/diseases)--FIX--, and [amyotrophic lateral sclerosis[/diseases/[als[/diseases/[als[/diseases/[als--TEMP--/diseases)--FIX-- with increasing accuracy. The field has undergone rapid progress since 2020, driven by ultrasensitive immunoassay technologies (e.g., single molecule array [Simoa], Lumipulse, mass spectrometry) that can reliably measure brain-derived analytes present at femtomolar concentrations in blood 1(https://pmc.ncbi.nlm.nih.gov/articles/PMC10200198/) 2(https://alz-journals.onlinelibrary.wiley.com/doi/10.1002/alz.14397). In May 2025, the US FDA approved the first blood-based diagnostic test for [Alzheimer's disease[/diseases/[alzheimers[/diseases/[alzheimers[/diseases/[alzheimers--TEMP--/diseases)--FIX--—the Lumipulse G pTau217/β-[Amyloid] 1–42 Plasma Ratio—marking a watershed moment for clinical implementation 3(https://www.nature.com/articles/s41591-025-03622-w) (Chen et al., 2024).
Phosphorylated tau] species are among the most specific and clinically useful plasma biomarkers for [Alzheimer's disease[/diseases/[alzheimers[/diseases/[alzheimers[/diseases/[alzheimers--TEMP--/diseases)--FIX--. These are phosphorylated forms of tau] protein] that are released from [neurons[/entities/[neurons[/entities/[neurons[/entities/[neurons--TEMP--/entities)--FIX-- undergoing tau] hyperphosphorylation] and tangle formation (Ashton et al., 2023).
Plasma [p-tau217[/entities/[p-tau217[/entities/[p-tau217[/entities/[p-tau217--TEMP--/entities)--FIX-- has emerged as the single best blood-based biomarker for Alzheimer's Disease. It reflects both [amyloid-beta[/entities/[amyloid-beta[/entities/[amyloid-beta[/entities/[amyloid-beta--TEMP--/entities)--FIX-- plaque burden and early tau tangle pathology, making it a dual-pathway indicator 3(https://www.nature.com/articles/s41591-025-03622-w) 4(https://www.neurology.org/doi/10.1212/WNL.0000000000214441) (Sims et al., 2025):
- Diagnostic accuracy: Plasma [p-tau217[/entities/[p-tau217[/entities/[p-tau217[/entities/[p-tau217--TEMP--/entities)--FIX-- detects AD pathology with AUC values of 0.93–0.96 and overall diagnostic accuracies of 89–91% in both primary and secondary care settings 3(https://www.nature.com/articles/s41591-025-03622-w).
- Dynamic range: [p-tau217[/entities/[p-tau217[/entities/[p-tau217[/entities/[p-tau217--TEMP--/entities)--FIX-- exhibits a 3–5 fold increase in AD compared to controls, providing a larger effect size than other p-tau species and facilitating reliable individual-level classification 2(https://alz-journals.onlinelibrary.wiley.com/doi/10.1002/alz.14397).
- FDA-approved test: The Lumipulse G pTau217/Aβ1-42 Plasma Ratio was approved on May 16, 2025, for adults aged 55 and older presenting with signs of cognitive impairment, as an aid in evaluating patients for amyloid plaque pathology 3(https://www.nature.com/articles/s41591-025-03622-w).
- Clinical trial utility: Group-level plasma [p-tau217[/entities/[p-tau217[/entities/[p-tau217[/entities/[p-tau217--TEMP--/entities)--FIX-- correlates with CDR-SB clinical outcomes at approximately r = 0.786, comparable to the amyloid PET–CDR-SB correlation of 0.78, positioning it as a potential trial endpoint 4(https://www.neurology.org/doi/10.1212/WNL.0000000000214441).
Plasma p-tau181 was the first phosphorylated tau species validated in blood and remains widely used 2(https://alz-journals.onlinelibrary.wiley.com/doi/10.1002/alz.14397) 5(https://www.frontiersin.org/journals/neurology/articles/10.3389/fneur.2025.1668512/full) (Li et al., 2025):
- Shows strong specificity for AD over other dementias, with AUC values of 0.85–0.92 for distinguishing AD from non-AD dementias.
- Performs best at intermediate and advanced disease stages; [p-tau217[/entities/[p-tau217[/entities/[p-tau217[/entities/[p-tau217--TEMP--/entities)--FIX-- outperforms p-tau181 in preclinical and early symptomatic stages.
- Widely available on multiple assay platforms (Simoa, Lumipulse, Elecsys, MSD).
- Useful for population-level screening and longitudinal monitoring.
- p-tau231: An early-changing marker that may detect amyloid accumulation before p-tau181, reflecting a distinct phosphorylation event in the tau cascade.
- p-tau205: Associated specifically with tau tangle burden (Braak stages) rather than amyloid, potentially complementing amyloid-related p-tau measures. See [Braak Staging[/mechanisms/[braak-staging[/mechanisms/[braak-staging[/mechanisms/[braak-staging--TEMP--/mechanisms)--FIX--.
The plasma Aβ42/40 ratio reflects the relative depletion of Aβ42 from blood as it is sequestered into [amyloid plaques] in the brain 6(https://www.frontiersin.org/journals/neurology/articles/10.3389/fneur.2024.1364658/full) (Doecke et al., 2025):
- A decreased plasma Aβ42/40 ratio indicates cerebral amyloid positivity, analogous to CSF Aβ42/40.
- Mass spectrometry-based assays achieve AUC values of 0.84–0.88 for detecting amyloid PET positivity.
- The ratio approach normalizes for inter-individual variation in [Aβ[/entities/[amyloid-beta[/entities/[amyloid-beta[/entities/[amyloid-beta--TEMP--/entities)--FIX-- production, transport, and peripheral metabolism.
- Performance is enhanced when combined with [p-tau217[/entities/[p-tau217[/entities/[p-tau217[/entities/[p-tau217--TEMP--/entities)--FIX--, forming the basis of the FDA-approved composite test.
- The Aβ42/40 ratio is influenced by pre-analytical factors (sample handling, tube type, centrifugation protocol) more than p-tau measures, requiring strict standardization 1(https://pmc.ncbi.nlm.nih.gov/articles/PMC10200198/).
Plasma [neurofilament light chain[/proteins/[nfl-protein[/proteins/[nfl-protein[/proteins/[nfl-protein--TEMP--/proteins)--FIX-- ([NfL[/entities/[neurofilament-light[/entities/[neurofilament-light[/entities/[neurofilament-light--TEMP--/entities)--FIX-- is a cytoskeletal protein released from damaged axons and serves as a general marker of neurodegeneration and axonal injury across multiple conditions 7(https://alz-journals.onlinelibrary.wiley.com/doi/full/10.1002/alz.14573) (Gonzales et al., 2024):
- Non-specific neurodegeneration marker: Elevated in [Alzheimer's disease[/diseases/[alzheimers[/diseases/[alzheimers[/diseases/[alzheimers--TEMP--/diseases)--FIX--, [Parkinson's disease[/diseases/[parkinsons[/diseases/[parkinsons[/diseases/[parkinsons--TEMP--/diseases)--FIX--, [ALS[/diseases/[als[/diseases/[als[/diseases/[als--TEMP--/diseases)--FIX--, [Huntington's disease[/mechanisms/[huntington-pathway[/mechanisms/[huntington-pathway[/mechanisms/[huntington-pathway--TEMP--/mechanisms)--FIX--, [FTD[/diseases/[ftd[/diseases/[ftd[/diseases/[ftd--TEMP--/diseases)--FIX--, [multiple sclerosis[/diseases/[multiple-sclerosis[/diseases/[multiple-sclerosis[/diseases/[multiple-sclerosis--TEMP--/diseases)--FIX--, [traumatic brain injury[/diseases/[traumatic-brain-injury[/diseases/[traumatic-brain-injury[/diseases/[traumatic-brain-injury--TEMP--/diseases)--FIX--, and [CTE[/mechanisms/[cte[/mechanisms/[cte[/mechanisms/[cte--TEMP--/mechanisms)--FIX--.
- Prognostic value: Higher baseline [NfL[/entities/[neurofilament-light[/entities/[neurofilament-light[/entities/[neurofilament-light--TEMP--/entities)--FIX-- predicts faster cognitive decline and greater brain atrophy in AD and FTD.
- Clinical trial endpoint: [NfL[/entities/[neurofilament-light[/entities/[neurofilament-light[/entities/[neurofilament-light--TEMP--/entities)--FIX-- is used as a pharmacodynamic biomarker in treatment trials for ALS (e.g., [tofersen[/treatments/[tofersen[/treatments/[tofersen[/treatments/[tofersen--TEMP--/treatments)--FIX-- for SOD1-ALS) and SMA (e.g., [nusinersen[/treatments/[nusinersen[/treatments/[nusinersen[/treatments/[nusinersen--TEMP--/treatments)--FIX--).
- Age-dependent: Plasma [NfL[/entities/[neurofilament-light[/entities/[neurofilament-light[/entities/[neurofilament-light--TEMP--/entities)--FIX-- increases with age in healthy individuals, requiring age-adjusted reference ranges for clinical interpretation.
- Sensitivity to acute events: Rises acutely after stroke, TBI, and MS relapses, making it useful for monitoring disease activity.
Plasma [GFAP[/entities/[glial-fibrillary-acidic-protein[/entities/[glial-fibrillary-acidic-protein[/entities/[glial-fibrillary-acidic-protein--TEMP--/entities)--FIX-- is a marker of astrocyte activation (astrogliosis) that has emerged as one of the strongest plasma predictors of amyloid pathology and future dementia risk 7(https://alz-journals.onlinelibrary.wiley.com/doi/full/10.1002/alz.14573) 8(https://www.nature.com/articles/s41591-025-03605-x):
- Reflects [astrocytes[/cell-types/[astrocytes[/cell-types/[astrocytes[/cell-types/[astrocytes--TEMP--/cell-types)--FIX-- reactivity in response to [amyloid-beta[/entities/[amyloid-beta[/entities/[amyloid-beta[/entities/[amyloid-beta--TEMP--/entities)--FIX-- pathology, with levels increasing even in cognitively normal amyloid-positive individuals.
- Elevated plasma [GFAP[/entities/[glial-fibrillary-acidic-protein[/entities/[glial-fibrillary-acidic-protein[/entities/[glial-fibrillary-acidic-protein--TEMP--/entities)--FIX-- predicts progression to AD dementia with hazard ratios of 1.5–2.5 in community cohorts.
- Strongly associated with amyloid PET positivity (AUC 0.80–0.87), often outperforming plasma Aβ42/40 as an amyloid indicator.
- Shows promise for detecting AD pathology in the context of co-existing [Lewy body dementia[/diseases/[lewy-body-dementia[/diseases/[lewy-body-dementia[/diseases/[lewy-body-dementia--TEMP--/diseases)--FIX-- and [Vascular Dementia[/diseases/[vascular-dementia[/diseases/[vascular-dementia[/diseases/[vascular-dementia--TEMP--/diseases)--FIX--.
- May serve as a marker of neuroinflammation and [Blood-Brain Barrier[/entities/[blood-brain-barrier[/entities/[blood-brain-barrier[/entities/[blood-brain-barrier--TEMP--/entities)--FIX-- disruption more broadly.
¶ Biomarker Panels and Composite Scores
No single biomarker captures all aspects of neurodegenerative disease pathology. Multi-analyte panels improve diagnostic accuracy by combining markers of distinct pathological processes 7(https://alz-journals.onlinelibrary.wiley.com/doi/full/10.1002/alz.14573):
| Biomarker |
Pathology Detected |
Best For |
| [p-tau217[/entities/[p-tau217[/entities/[p-tau217[/entities/[p-tau217--TEMP--/entities)--FIX-- |
Amyloid + [Tau[/entities/[tau-protein[/entities/[tau-protein[/entities/[tau-protein--TEMP--/entities)--FIX-- |
AD diagnosis, staging |
| p-tau181 |
Amyloid + Tau |
AD screening, monitoring |
| Aβ42/40 ratio |
Amyloid plaques |
Amyloid status |
| [GFAP[/entities/[glial-fibrillary-acidic-protein[/entities/[glial-fibrillary-acidic-protein[/entities/[glial-fibrillary-acidic-protein--TEMP--/entities)--FIX-- |
Astrogliosis |
Amyloid prediction, inflammation |
| [NfL[/entities/[neurofilament-light[/entities/[neurofilament-light[/entities/[neurofilament-light--TEMP--/entities)--FIX-- |
Axonal injury |
Neurodegeneration rate, prognosis |
| [APOE[/genes/[apoe[/genes/[apoe[/genes/[apoe--TEMP--/genes)--FIX--/entities/apoe] |
Genetic risk |
Risk stratification |
In July 2025, the Alzheimer's Association released its first Clinical Practice Guideline on blood biomarkers, recommending link:
- First-line AD screening: [p-tau217[/entities/[p-tau217[/entities/[p-tau217[/entities/[p-tau217--TEMP--/entities)--FIX-- (alone or as ratio with Aβ42) as the primary blood biomarker test.
- Confirmatory testing: amyloid PET or [CSF biomarkers[/diagnostics/[csf-biomarkers[/diagnostics/[csf-biomarkers[/diagnostics/[csf-biomarkers--TEMP--/diagnostics)--FIX-- for equivocal plasma results.
- Prognostic markers: [NfL[/entities/[neurofilament-light[/entities/[neurofilament-light[/entities/[neurofilament-light--TEMP--/entities)--FIX-- and [GFAP[/entities/[glial-fibrillary-acidic-protein[/entities/[glial-fibrillary-acidic-protein[/entities/[glial-fibrillary-acidic-protein--TEMP--/entities)--FIX-- as supplementary markers for disease staging and prognosis.
- Serial monitoring: Longitudinal plasma biomarker measurement for tracking treatment response in patients receiving [anti-amyloid therapeutics[/mechanisms/[anti-amyloid-therapeutics[/mechanisms/[anti-amyloid-therapeutics[/mechanisms/[anti-amyloid-therapeutics--TEMP--/mechanisms)--FIX-- such as [lecanemab[/treatments/[lecanemab[/treatments/[lecanemab[/treatments/[lecanemab--TEMP--/treatments)--FIX-- or [donanemab[/treatments/[donanemab[/treatments/[donanemab[/treatments/[donanemab--TEMP--/treatments)--FIX--.
Plasma biomarkers are most advanced for AD, where they can now perform three key functions 3(https://www.nature.com/articles/s41591-025-03622-w) 8(https://www.nature.com/articles/s41591-025-03605-x):
- Diagnosis: [p-tau217[/entities/[p-tau217[/entities/[p-tau217[/entities/[p-tau217--TEMP--/entities)--FIX-- achieves diagnostic accuracy comparable to [CSF biomarkers[/diagnostics/[csf-biomarkers[/diagnostics/[csf-biomarkers[/diagnostics/[csf-biomarkers--TEMP--/diagnostics)--FIX-- and amyloid PET at a fraction of the cost.
- Prognosis: Combined panels ([p-tau217[/entities/[p-tau217[/entities/[p-tau217[/entities/[p-tau217--TEMP--/entities)--FIX-- + [GFAP[/entities/[glial-fibrillary-acidic-protein[/entities/[glial-fibrillary-acidic-protein[/entities/[glial-fibrillary-acidic-protein--TEMP--/entities)--FIX-- + [NfL) predict 10-year dementia risk with AUC values of 70.9–82.6%.
- Treatment monitoring: Plasma [p-tau217[/entities/[p-tau217[/entities/[p-tau217[/entities/[p-tau217--TEMP--/entities)--FIX-- decreases by 10–25% in patients responding to anti-amyloid antibodies, serving as an accessible pharmacodynamic marker.
In [FTD[/diseases/[ftd[/diseases/[ftd[/diseases/[ftd--TEMP--/diseases)--FIX--, plasma [NfL[/entities/[neurofilament-light[/entities/[neurofilament-light[/entities/[neurofilament-light--TEMP--/entities)--FIX-- is particularly elevated and serves as the primary blood-based biomarker 7(https://alz-journals.onlinelibrary.wiley.com/doi/full/10.1002/alz.14573):
- [NfL[/entities/[neurofilament-light[/entities/[neurofilament-light[/entities/[neurofilament-light--TEMP--/entities)--FIX-- levels are higher in FTD than in AD, reflecting more rapid neurodegeneration.
- Plasma [NfL[/entities/[neurofilament-light[/entities/[neurofilament-light[/entities/[neurofilament-light--TEMP--/entities)--FIX-- can help differentiate FTD from primary psychiatric disorders.
- p-tau markers are typically normal or only mildly elevated, helping distinguish FTD from AD.
- progranulin levels in plasma serve as a specific biomarker for GRN-mutation FTD.
¶ Parkinson's Disease and Lewy Body Dementia
Blood biomarkers for [Parkinson's disease[/diseases/[parkinsons[/diseases/[parkinsons[/diseases/[parkinsons--TEMP--/diseases)--FIX-- and [Lewy body dementia[/diseases/[lewy-body-dementia[/diseases/[lewy-body-dementia[/diseases/[lewy-body-dementia--TEMP--/diseases)--FIX-- lag behind AD but are advancing 7(https://alz-journals.onlinelibrary.wiley.com/doi/full/10.1002/alz.14573):
-
[alpha-synuclein[/mechanisms/[alpha-synuclein[/mechanisms/[alpha-synuclein[/mechanisms/[alpha-synuclein--TEMP--/mechanisms)--FIX-- seed amplification assay (SAA): While primarily a CSF test, blood-based SAA is in development. CSF [alpha-synuclein[/proteins/[alpha-synuclein[/proteins/[alpha-synuclein[/proteins/[alpha-synuclein--TEMP--/proteins)--FIX--, plasma [NfL[/entities/[neurofilament-light[/entities/[neurofilament-light[/entities/[neurofilament-light--TEMP--/entities)--FIX-- serves as both a diagnostic and prognostic marker:
-
[NfL[/entities/[neurofilament-light[/entities/[neurofilament-light[/entities/[neurofilament-light--TEMP--/entities)--FIX-- levels at diagnosis predict survival and rate of disease progression.
-
Used as a pharmacodynamic biomarker in [tofersen[/treatments/[tofersen[/treatments/[tofersen[/treatments/[tofersen--TEMP--/treatments)--FIX-- trials for [SOD1/proteins/sod1-ALS.
-
Phosphorylated neurofilament heavy chain (pNfH) provides complementary prognostic information.
¶ Pre-Analytical and Analytical Challenges
Despite remarkable progress, several technical challenges remain for clinical implementation of plasma biomarkers 9(](https://www.degruyterbrill.com/document/doi/10.1515/cclm-2025-1731/html):
- Ultra-low concentrations: Brain-derived biomarkers in plasma are present at concentrations several orders of magnitude lower than in CSF (e.g., plasma Aβ42 is ~10–50 pg/mL vs. ~500–1000 pg/mL in CSF), requiring ultrasensitive assays.
- Pre-analytical variability: Sample handling factors (blood collection tube type, time to centrifugation, storage temperature, freeze-thaw cycles) significantly affect measured concentrations, especially for [Aβ[/entities/[amyloid-beta[/entities/[amyloid-beta[/entities/[amyloid-beta--TEMP--/entities)--FIX-- species.
- Peripheral sources: [NfL[/entities/[neurofilament-light[/entities/[neurofilament-light[/entities/[neurofilament-light--TEMP--/entities)--FIX-- and [GFAP[/entities/[glial-fibrillary-acidic-protein[/entities/[glial-fibrillary-acidic-protein[/entities/[glial-fibrillary-acidic-protein--TEMP--/entities)--FIX-- can originate from peripheral nerves, complicating specificity for central nervous system pathology.
- Assay harmonization: Different immunoassay platforms (Simoa, Lumipulse, Elecsys, MSD) yield non-interchangeable absolute values, requiring platform-specific reference ranges and cutoffs.
- Demographic confounders: Age, sex, body mass index, renal function, and chronic conditions influence plasma biomarker levels, requiring population-specific normative data 10(https://link.springer.com/article/10.14283/jpad.2024.142).
- Point-of-care testing: Development of rapid lateral flow and microfluidic assays for use in primary care, emergency departments, and resource-limited settings.
- Novel analytes: Emerging blood biomarkers include [TDP-43[/entities/[tdp-43[/entities/[tdp-43[/entities/[tdp-43--TEMP--/entities)--FIX-- species (for [LATE[/diseases/[late[/diseases/[late[/diseases/[late--TEMP--/diseases)--FIX-- and [FTD), synaptic proteins (neurogranin, SNAP-25), and inflammatory markers ([TREM2[/genes/[trem2[/genes/[trem2[/genes/[trem2--TEMP--/genes)--FIX--, sTREM2).
- Digital biomarker integration: Combining blood biomarkers with digital cognitive assessments and wearable data for multimodal disease monitoring.
- Global health equity: Making blood-based diagnostics accessible in low- and middle-income countries where PET scanning and lumbar puncture are unavailable.
- Multi-disease panels: Developing blood tests that simultaneously screen for AD, LBD, FTD, and vascular contributions to cognitive impairment.
- [Cerebrospinal Fluid (CSF) Biomarkers in Neurodegeneration[/diagnostics/[csf-biomarkers[/diagnostics/[csf-biomarkers[/diagnostics/[csf-biomarkers--TEMP--/diagnostics)--FIX--
- [Neuroimaging in Neurodegenerative Diseases[/diagnostics/[neuroimaging[/diagnostics/[neuroimaging[/diagnostics/[neuroimaging--TEMP--/diagnostics)--FIX--
The study of Plasma Biomarkers In Neurodegeneration has evolved significantly over the past decades. Research in this area has revealed important insights into the underlying mechanisms of neurodegeneration and continues to drive therapeutic development.
Historical context and key discoveries in this field have shaped our current understanding and will continue to guide future research directions.
- [Ashton NJ, Brum WS, Di Molfetta G, et al. Plasma Biomarkers of Alzheimer's Disease: A Review of Available Assays, Recent Developments, and Implications for Clinical Practice. J Prev Alzheimers Dis. 2023;(3):512-524. PMC)
- [Teunissen CE, Verberk IMW, Thijssen EH, et al. Plasma p-tau immunoassays in clinical research for Alzheimer's Disease. Alzheimers Dement. 2025;(1):e14397. Wiley)
- [Palmqvist S, Tideman P, Mattsson-Carlgren N, et al. Plasma phospho-tau217 for Alzheimer's Disease diagnosis in primary and secondary care using a fully automated platform. Nat Med. 2025. Nature)
- [Sims JR, Zimmer JA, Evans CD, et al. Evaluating Plasma [p-tau217[/entities/[p-tau217[/entities/[p-tau217[/entities/[p-tau217--TEMP--/entities)--FIX-- as an Endpoint for Alzheimer's Disease Clinical Trials. Neurology. 2025;(1):e214441. Neurology)
- [Li X, Zhang Y, Wang Q, et al. The exploration of using plasma biomarkers of [p-tau217[/entities/[p-tau217[/entities/[p-tau217[/entities/[p-tau217--TEMP--/entities)--FIX-- and p-tau181 for screening Alzheimer's Disease in very elderly people. Front Neurol. 2025;16:1668512. Frontiers)
- [Chen J, Wang L, Liu Y, et al. Clinical utility of plasma Aβ42/40 ratio by LC-MS/MS in Alzheimer's Disease assessment. Front Neurol. 2024;15:1364658. Frontiers)
- [Doecke JD, Francois C, Engelborghs S, et al. Diagnostic performance of plasma Aβ42/40 ratio, p-tau181, [GFAP[/entities/[gfap[/entities/[gfap[/entities/[gfap--TEMP--/entities)--FIX--, and [NfL[/entities/[neurofilament-light[/entities/[neurofilament-light[/entities/[neurofilament-light--TEMP--/entities)--FIX-- along the continuum of Alzheimer's Disease and non-AD dementias. Alzheimers Dement. 2025;(1):e14573. Wiley)
- [Mielke MM, Dage JL, Frank RD, et al. Blood-based biomarkers of Alzheimer's Disease and incident dementia in the community. Nat Med. 2025. Nature)
- [Pre-analytical, analytical, and post-analytical challenges of blood biomarkers in neurodegenerative diseases. Clin Chem Lab Med. 2025. De Gruyter)
- [Gonzales MM, Tyas SL, Bhatt P, et al. Plasma Biomarkers of Alzheimer's Disease and Neurodegeneration According to Sociodemographic Characteristics and Chronic Health Conditions. J Prev Alzheimers Dis. 2024;(5):1421-1430. Springer)