Every row of the evidence table

A threshold-derivation meta-analysis: it converges on 18 Centiloids (data-driven) and 27 Centiloids (visual reads) and flags 11-26 as a range to read with caution. It compares no exposure, so no direction exists to record.

Appropriate use criteria rated by consensus: for amyloid PET seven of 17 scenarios were rated appropriate, two uncertain and eight rarely appropriate; for tau PET five, six and six. No effect estimate is reported.

Direction is for higher baseline plasma p-tau217 in cognitively unimpaired women: each SD increase more than doubled the hazard of MCI or dementia. Associations were larger in women over 70, APOE4 carriers and White women, and p-tau217 was not associated with incident MCI in Black women.

Direction is for the test's accuracy against the reference standard; an accuracy result, not a health outcome. The estimated age at plasma %p-tau217 positivity predicted age at symptom onset (adjusted R2 0.337-0.612) with a median absolute error of 3.0-3.7 years, which the authors call acceptable for trials but not yet for individual clinical use.

Direction is for higher baseline plasma p-tau217 in cognitively unimpaired adults: each SD raised the hazard of progression by 38%, and the very-high group had a 38% absolute 5-year risk of progression.

Direction is for higher plasma p-tau217: each SD raised the hazard of incident cognitive impairment by 41%, more steeply in APOE-ε4 carriers (76%) than non-carriers (26%), with survival curves separating 3-4 years after the blood test.

Direction is for the test's accuracy against the reference standard; an accuracy result, not a health outcome. Stand-alone plasma p-tau217 gave 81% accuracy and 79% PPV; confirming positives with PET or CSF raised both to 91% while cutting PET scans needed to find 100 amyloid-positive people from 536 to 124. Immunoassays matched mass spectrometry on PPV but had lower accuracy.

Direction is for the test's accuracy against the reference standard; an accuracy result, not a health outcome. Combined plasma %p-tau217 and Aβ42/40 detected abnormal CSF amyloid status (AUC 0.949) and each predicted rising amyloid PET over time in people who started below the positivity threshold, replicated in two further cohorts; p-tau231 and GFAP added no clear independent value.

Direction is for the test's accuracy against the reference standard; an accuracy result, not a health outcome. All four assays (Lumipulse, Johnson & Johnson, ALZpath, NULISA) gave statistically equivalent AUCs of 0.84-0.90 for amyloid positivity, with cross-platform correlations of 0.40-0.86.

An editorial reviewing the FDA clearance of the Lumipulse plasma ratio test. It relays performance figures from the FDA summary and other studies and reports no data of its own.

Direction is for the blood test's ability to detect treatment-related amyloid clearance on PET: AUC 0.61, which the authors call suboptimal and not currently usable for that purpose. It says nothing about the drug's effect.

Direction is for the test's accuracy against the reference standard; an accuracy result, not a health outcome. Among p-tau217-positive patients, a positive eMTBR-tau243 identified clinically established Alzheimer's disease with 81% accuracy and predicted faster cognitive decline and tau accumulation.

Direction is for the test's accuracy against the reference standard; an accuracy result, not a health outcome. Subgroup-specific optimal cutoffs and a double-cutoff strategy both improved accuracy over the standard single cutoff, most markedly in chronic kidney disease (0.65 to 0.83) and anaemia.

The review's own summary points two ways: CSF biomarker tests were mostly cost-effective against cognitive assessment or imaging, while blood biomarker tests showed mixed results; every included study was model-based.

The findings point two ways: the p-tau217/Aβ42 ratio tracked AD-related factors (MCI, AD dementia, future progression, age, APOE ε4) more closely than either marker alone and had few intermediate results, but it was also related to kidney function, diabetes and hearing loss, and medical morbidities were most frequent among intermediate classifications.

Direction is for the test's accuracy against the reference standard; an accuracy result, not a health outcome. The prespecified APS2 cut point gave 91% accuracy, 90% sensitivity and 92% specificity against amyloid PET.

Direction is for the test's accuracy against the reference standard; an accuracy result, not a health outcome. Plasma p-tau217 detected amyloid PET positivity with 82% sensitivity and 86% specificity, comparable to CSF p-tau217; less sensitive for tau PET.

Direction is for the test's accuracy against the reference standard; an accuracy result, not a health outcome. AUC 0.93-0.96; accuracy 89-91% in secondary care and 85% in primary care, lower (83%) at age 80 or older; a two-cutoff approach raised accuracy to 92-94% at the cost of 12-17% intermediate results.

Direction is for the test's accuracy against the reference standard; an accuracy result, not a health outcome. Plasma p-tau217 was the best-performing marker (88.1% sensitivity, 88.7% specificity, AUROC 91.1%, moderate certainty), ahead of p-tau181 and p-tau231; about 90% of studies were at high risk of bias.

Direction is for the test's accuracy against the reference standard; an accuracy result, not a health outcome. The Pitt-p-tau217 assay separated PSEN1 carriers from controls (AUC 0.94) and amyloid PET-positive from -negative cognitively normal adults (AUC up to 0.84), equivalent to the ALZpath assay.

A clinical practice guideline. It sets performance thresholds for blood tests (at least 90% sensitivity and 75% specificity for triage; at least 90% for both to substitute for amyloid PET or CSF) and reports no effect estimate of its own.

Direction is for the test's accuracy against the reference standard; an accuracy result, not a health outcome. Performance varied widely across tests, from 49.3% to 91.4% pooled sensitivity and 61.5% to 96.7% pooled specificity at a single cut-point, with most studies at high risk of bias.

Direction is for the test's accuracy against the reference standard; an accuracy result, not a health outcome. All p-tau217 tests detected abnormal amyloid PET (AUC 0.91-0.96) and tau PET (0.94-0.97); the mass-spectrometry %p-tau217 ratio was best (accuracy 0.93 versus 0.83-0.88 for immunoassays) and is proposed as a stand-alone confirmatory test, with immunoassays better suited to triage.

Direction is for the test's accuracy against the reference standard; an accuracy result, not a health outcome. The Lumipulse plasma p-tau217/Aβ42 ratio reached AUC 0.963-0.966 for amyloid PET and 0.947-0.974 for tau PET, equivalent to CSF tests and better than plasma p-tau217 alone, with fewer intermediate results.

Direction is for the test's accuracy against the reference standard; an accuracy result, not a health outcome. Plasma p-tau217/Aβ42 had the highest accuracy (0.88 in Black and 0.91 in White participants) and fewest intermediate results, with no difference in classification by race.

Direction is for chronic kidney disease as a source of false signal: at eGFR 45 versus 60, p-tau217 was 31-55% higher in amyloid-negative people on two immunoassays, a rise largely removed by using the %p-tau217 ratio. A test-validity result, not a health outcome.

Direction is for the test's accuracy against the reference standard; an accuracy result, not a health outcome. Plasma p-tau217 identified symptomatic AD with 95% sensitivity and 82% specificity (86% with the Aβ42 ratio) and tracked CSF biomarkers closely (AUC 0.94-0.96); reduced kidney function raised levels in patients without AD.

A price-threshold model: it estimates the test price at which diagnostic cost per true-positive case equals standard care ($290-$1,950 depending on use), and compares no actual price against it, so there is no direction to record.

Direction is for the test's accuracy against the reference standard; an accuracy result, not a health outcome. The APS2 blood test reached AUC 0.96-0.97 and 88-92% accuracy, and its 91% accuracy for clinical AD beat primary care physicians (61%) and dementia specialists (73%).

Direction is for the test's accuracy against the reference standard; an accuracy result, not a health outcome. APS2 gave AUC 0.94 and 88% agreement with amyloid PET, with similar performance by ethnicity, sex, age and APOE4 status.

Direction is for the test's accuracy against the reference standard; an accuracy result, not a health outcome. The ALZpath plasma p-tau217 immunoassay reached AUC 0.92-0.96 for amyloid and 0.93-0.97 for tau across three cohorts, comparable with CSF, and a three-range cut-off cut confirmatory testing by about 80%.

Direction is for the test's accuracy against the reference standard; an accuracy result, not a health outcome. Plasma p-tau217 identified amyloid positivity with AUC 0.94; a two-cut-point rule sent only 17% for CSF or PET (sensitivity 0.94, specificity 0.86), and among amyloid-positive people it identified high tau load (AUC 0.92), potentially avoiding 56.9% of tau-PET scans.

A workgroup recommendations document. It sets target sensitivity and specificity for blood biomarker tests (≥90% / ≥85% for triage in primary care; ~90% / ~90% as a confirmatory test) and reports no data of its own.

Direction is for the test's accuracy against the reference standard; an accuracy result, not a health outcome. A blood model of p-tau217, age and APOE ε4 (AUC 89.3% development, 94.3% validation) used to triage patients gave 88-92% overall accuracy while cutting confirmatory CSF tests by 61-86%.

Direction is for disclosing the blood panel during multidisciplinary meetings: median diagnostic confidence rose from 80% to 90%, though the suspected etiology changed in only 5% of patients and the syndrome diagnosis in 1%. Against CSF/PET, high- and low-probability results identified 76% of amyloid positives and 85% of negatives.

The results point different ways: diagnostic confidence rose 1.43 points, but diagnosis changed in only 17.2% and management in 27.7%, below the 30% threshold the investigators set as clinically significant; a non-elevated result reduced amyloid PET use, and patients with elevated results had higher anxiety at 2-3 months.

The findings point different ways: lower eGFR raised every blood biomarker except Aβ42/40 (a test-interpretation caveat), yet impaired kidney function did not itself raise dementia risk (HR 0.93), while the association between high NfL and dementia was about twice as strong in people with impaired kidneys.

Direction is for the blood test's prognostic performance: plasma p-tau217 predicted cognitive decline and progression to MCI as well as tau PET (R2 0.33 vs 0.34; HR 1.57 vs 1.61), and using the blood test first cut the number needed to screen for a trial by 94%. A prognostic-performance result, not a health outcome.

Direction is for abnormal baseline plasma p-tau217: people positive for both plasma amyloid and tau progressed to MCI at 7.8 times the rate of those negative for both, and tau-positive/amyloid-negative people at 4.3 times. CSF and PET gave similar results; adding plasma Aβ42/40 did not improve prediction.

The two measures behaved differently: baseline plasma p-tau217 predicted later cognitive decline about as well as entorhinal tau PET (ρ -0.47 vs -0.55), but over time p-tau217 rose then decelerated and tracked concurrent cognitive change only weakly (ρ -0.24) or not at all in the PET substudy, whereas regional tau PET change correlated strongly with concurrent decline.

Direction is for higher baseline plasma GFAP in cognitively unimpaired adults: it predicted faster cognitive decline, CDR progression, cortical atrophy and conversion to amyloid positivity, with stronger effects in females.

Direction is for higher plasma pTau217: it was associated with global and domain-specific cognitive decline within both racial groups and discriminated 3-year dementia well (AUC 0.81 in Black and 0.77 in White adults); biomarker levels were similar across races and the association with decline was similar, though pTau217 tracked faster global and semantic memory decline in Black adults.

Direction is for adverse biomarker levels: only the Alzheimer-specific markers measured in midlife (lower Aβ42:Aβ40, higher p-tau181) predicted dementia two decades later, while every marker measured in late life did, NfL most strongly (HR 1.92 per SD). Biomarkers changed faster in APOE ε4 carriers and with midlife hypertension or diabetes.

Direction is for high serum NfL or GFAP: the top tertile of either raised incident dementia risk by 38-49% and roughly tripled dementia-specific mortality; being in the top tertile of both doubled dementia risk and raised dementia mortality nine-fold. NfL was independently associated with faster cognitive decline.

Direction is for astrocyte reactivity: amyloid was associated with higher plasma p-tau only in people positive for astrocyte reactivity, and an AD-like pattern of tau-PET accumulation as a function of amyloid appeared only in those individuals, cross-sectionally and longitudinally.

Direction is for a rising serum NfL: its rate of change separated mutation carriers from non-carriers 16.2 years before expected symptom onset (versus 6.8 years for a single level), peaked around symptom conversion, and predicted cortical thinning and cognitive decline.

Direction is for microglial activation: amyloid was associated with astrocyte reactivity across cortical regions only when microglia were activated, and that microglia-dependent reactivity related to cognitive impairment through tau phosphorylation and aggregation.

Direction is for the test's accuracy against the reference standard; an accuracy result, not a health outcome. The two-marker plasma model matched PET-based stages with a C index of 0.91 in both the derivation and validation cohorts, tracked clinical stage (C index 0.84-0.86) and aligned with autopsy ADNC (AUC 0.96), improving on %p-tau217 alone at the intermediate stage.

Direction is for the test's accuracy against the reference standard; an accuracy result, not a health outcome. Plasma Aβ42/40, p-tau217, p-tau181 and NfL classified AD with AUC 83% and FTLD with 88%, consistent across countries, rising to 89% and 95% when combined with neuroimaging patterns and cognitive measures.

The three markers pointed different ways: plasma p-tau217 distinguished amyloid/tau stages, GFAP tracked amyloid-driven tau progression, and NfL was only weakly linked to Alzheimer pathology and, in the authors' words, inadequate as a neuronal injury biomarker for AD.