Concept
Alzheimer’s and MCI markers
12 studies
Alzheimer’s disease and mild cognitive impairment are tracked with overlapping but not identical markers—blood proteins that forecast later dementia, CSF/PET tau that tracks early brain change, and behavioural tasks that separate biomarker-defined MCI from controls. This page states which claim each study supports.
Students meet “Alzheimer’s biomarkers” as one story. In practice, a plasma prognostic marker, a PET decline predictor, a connectome pattern, and a VR navigation task answer different questions. Mixing them invents false agreement.
Studies
12
Findings
12
12 supporting · 0 challenging · 21 qualifying citations
Open tensions
4
Currently
What we know
- Blood GFAP and NfL associate with higher later dementia risk years before diagnosis.
- In people with Alzheimer’s, tau and microglial PET can flag who declines faster.
- Tau tends to sit in network hubs and tracks weaker cortical connectivity in AD.
- A VR navigation task can separate biomarker-positive MCI from controls.
- Higher CSF tau can track early object-memory and hippocampal activity changes.
Largest unresolved question
Plasma GFAP/NfL forecast registry dementia years later in a volunteer cohort; tau/inflammation PET predict short-horizon decline in people already diagnosed with AD. Both can be valid—the limit is not treating prognosis and clinic decline as one assay.
Common misconceptions
A raised blood NfL or GFAP level diagnoses Alzheimer’s disease on its own.
These proteins are nonspecific injury/inflammation signals that associate with later dementia risk in cohorts; they are not a same-day AD rule-in test and rise in other neurological conditions.
All MCI is early Alzheimer’s, so any MCI marker equals an AD diagnosis.
Biomarker-positive and biomarker-negative MCI can look different on the same VR task; MCI is a clinical stage that needs biomarker and clinical context, not a single label.
A plasma AD panel with AUC 0.81 can replace CSF/PET or autopsy for diagnosis.
The Cardiff models discriminated clinical diagnosis from older controls; the authors note a substantial fraction of clinical AD lacks AD pathology at autopsy, and novel GWAS hits need replication.
Tau-laden retinal ganglion cells already amount to an in-clinic eye-scan biomarker.
The RGC findings are postmortem histology correlated with brain pathology. They motivate imaging research; they do not validate a living-patient diagnostic test.
Plasma p-tau217 AUC 0.96 means a blood test can replace PET everywhere.
The Geneva cut-offs came from one memory clinic; CSF comparison n=36, and transportability to other assays/labs is unproven.
Related
Claim ledger
What the evidence shows
Drawn from 12 studies in this library. Mix labels say which citation roles are present; they are not a strength score. Supports means evidence for a finding; Challenges means evidence against a stated position; Qualifies marks scope.
Blood GFAP and NfL associate with higher later dementia risk years before diagnosis.
In UK Biobank adults with baseline plasma measures, higher GFAP and NfL associated with roughly doubled hazards of incident all-cause dementia over ~13 years, with elevations detectable up to about 15 years before diagnosis and incremental prediction beyond demographic risk scores.
- Using Brain Scans to Predict Cognitive Decline in Alzheimer's— different question — short-horizon decline in diagnosed AD, not biobank prognosis
- Does brain tau protein affect object memory in older adults?— different compartment — CSF tau + fMRI, not plasma GFAP/NfL
- Can blood markers and genes diagnose Alzheimer’s?— clinic case-control discrimination with a multi-marker + APOE/PRS panel — not UK Biobank incident-dementia prognosis
Study Role Design N Population Outcome Blood GFAP and NfL predict dementia years ahead Supports CohortUK Biobank prospective plasma GFAP/NfL with registry dementia follow-up N=48542 · 1,312 incident all-cause dementia over ~13 years UK Biobank adults with baseline Olink plasma GFAP and NfL Incident all-cause dementia / ADRD HRs and prediction AUC for GFAP and NfL Using Brain Scans to Predict Cognitive Decline in Alzheimer's Qualifiesdifferent question — short-horizon decline in diagnosed AD, not biobank prognosis CohortBaseline MRI/PET (tau, microglial activation, atrophy) predicting 3-year cognitive decline N=55 · 26 Alzheimer’s-pathology patients (12 dementia, 14 amnestic MCI) and 29 healthy controls Patients with Alzheimer’s pathology and healthy controls with longitudinal cognition Baseline tau and microglial activation predicting decline; atrophy adding no independent value Does brain tau protein affect object memory in older adults? Qualifiesdifferent compartment — CSF tau + fMRI, not plasma GFAP/NfL OtherObservational CSF biomarker–fMRI association study; no assigned exposure N=21 · 21 cognitively unimpaired older adults analysed after spinal tap and mnemonic discrimination fMRI Cognitively unimpaired older adults Object mnemonic discrimination and hippocampal activation vs CSF tau Can blood markers and genes diagnose Alzheimer’s? Qualifiesclinic case-control discrimination with a multi-marker + APOE/PRS panel — not UK Biobank incident-dementia prognosis Case-controlAD Cardiff Cohort cases vs screened elderly controls; Simoa plasma biomarkers plus GWAS/PRS; clinical diagnosis not CSF/PET-confirmed. N=1947 · 1,439 AD cases (mean age 68) and 508 controls (mean age 82); 1,947 with APOE and genome-wide genotypes. Early- and late-onset sporadic Alzheimer’s disease cases and screened elderly controls from the Alzheimer’s Disease Cardiff Cohort. Discrimination of clinical AD (AUC) by plasma Aβ40/42, P-tau181, NfL, GFAP plus APOE/PRS, and GWAS of biomarkers. In people with Alzheimer’s, tau and microglial PET can flag who declines faster.
In longitudinal AD imaging, baseline tau PET burden and microglial activation predicted subsequent cognitive decline; when markers were modelled together, posterior cortical tau and inflammation carried prediction while atrophy added little incremental signal.
- Blood GFAP and NfL predict dementia years ahead— different population — volunteer biobank prognosis, not clinic AD decline
Study Role Design N Population Outcome Using Brain Scans to Predict Cognitive Decline in Alzheimer's Supports CohortBaseline MRI/PET (tau, microglial activation, atrophy) predicting 3-year cognitive decline N=55 · 26 Alzheimer’s-pathology patients (12 dementia, 14 amnestic MCI) and 29 healthy controls Patients with Alzheimer’s pathology and healthy controls with longitudinal cognition Baseline tau and microglial activation predicting decline; atrophy adding no independent value Blood GFAP and NfL predict dementia years ahead Qualifiesdifferent population — volunteer biobank prognosis, not clinic AD decline CohortUK Biobank prospective plasma GFAP/NfL with registry dementia follow-up N=48542 · 1,312 incident all-cause dementia over ~13 years UK Biobank adults with baseline Olink plasma GFAP and NfL Incident all-cause dementia / ADRD HRs and prediction AUC for GFAP and NfL Tau tends to sit in network hubs and tracks weaker cortical connectivity in AD.
In Alzheimer’s disease, tau PET burden concentrated in highly connected cortical hubs and higher overall tau associated with weakened cortical connection strength; progressive-supranuclear-palsy patterns differed, showing disease-specific mapping of tau onto networks.
- Using Brain Scans to Predict Cognitive Decline in Alzheimer's— related PET tau story, but decline prediction rather than connectome mapping
- Does Alzheimer’s tau hit retinal ganglion cells early?— postmortem retinal pS396/oligomeric tau in RGCs — not cortical tau PET connectome mapping
Study Role Design N Population Outcome How tau buildup shapes brain networks in dementia Supports Case-controlTau PET and functional connectome in Alzheimer's disease vs progressive supranuclear palsy N=34 · 17 AD and 17 PSP Patients with Alzheimer's disease or progressive supranuclear palsy who had capacity to consent Relationship of tau burden to the functional connectome in AD versus PSP Using Brain Scans to Predict Cognitive Decline in Alzheimer's Qualifiesrelated PET tau story, but decline prediction rather than connectome mapping CohortBaseline MRI/PET (tau, microglial activation, atrophy) predicting 3-year cognitive decline N=55 · 26 Alzheimer’s-pathology patients (12 dementia, 14 amnestic MCI) and 29 healthy controls Patients with Alzheimer’s pathology and healthy controls with longitudinal cognition Baseline tau and microglial activation predicting decline; atrophy adding no independent value Does Alzheimer’s tau hit retinal ganglion cells early? Qualifiespostmortem retinal pS396/oligomeric tau in RGCs — not cortical tau PET connectome mapping Case-controlHuman donor retina/brain comparison of AD dementia, MCI due to AD, and cognitively normal controls N=41 · AD dementia n=15, MCI due to AD n=10, CN controls n=16 Human retinal superior-temporal cross-sections and matched brain donors spanning MCI due to AD, AD dementia, and CN controls Pathogenic tau in RGCs (pS396-tau, oligomeric tau), RGC loss/morphology, and correlations with brain AD pathology and cognition A VR navigation task can separate biomarker-positive MCI from controls.
An entorhinal-cortex–based virtual navigation task produced larger path errors in MCI than controls, with biomarker-positive MCI performing worse than biomarker-negative MCI—linking a behavioural assay to CSF Alzheimer’s markers.
- Does brain tau protein affect object memory in older adults?— different behavioural assay — object mnemonic discrimination, not VR path error
Study Role Design N Population Outcome Using Virtual Reality to Detect Early Alzheimer's Disease Supports Cross-sectionalImmersive VR navigation test comparing biomarker-defined MCI patients and healthy controls N=86 · 45 MCI patients (12 biomarker-positive, 14 biomarker-negative among CSF-tested) and 41 healthy controls Mild cognitive impairment patients and healthy controls performing entorhinal-based VR navigation Navigation error distinguishing biomarker-positive early Alzheimer’s MCI from biomarker-negative MCI and controls Does brain tau protein affect object memory in older adults? Qualifiesdifferent behavioural assay — object mnemonic discrimination, not VR path error OtherObservational CSF biomarker–fMRI association study; no assigned exposure N=21 · 21 cognitively unimpaired older adults analysed after spinal tap and mnemonic discrimination fMRI Cognitively unimpaired older adults Object mnemonic discrimination and hippocampal activation vs CSF tau Higher CSF tau can track early object-memory and hippocampal activity changes.
In cognitively unimpaired older adults, higher CSF tau correlated with worse object mnemonic discrimination and greater right hippocampal task fMRI activity—evidence that a fluid marker can track early functional change before a dementia diagnosis.
- Blood GFAP and NfL predict dementia years ahead— different scale — biobank plasma prognosis, not small fMRI sample
Study Role Design N Population Outcome Does brain tau protein affect object memory in older adults? Supports OtherObservational CSF biomarker–fMRI association study; no assigned exposure N=21 · 21 cognitively unimpaired older adults analysed after spinal tap and mnemonic discrimination fMRI Cognitively unimpaired older adults Object mnemonic discrimination and hippocampal activation vs CSF tau Blood GFAP and NfL predict dementia years ahead Qualifiesdifferent scale — biobank plasma prognosis, not small fMRI sample CohortUK Biobank prospective plasma GFAP/NfL with registry dementia follow-up N=48542 · 1,312 incident all-cause dementia over ~13 years UK Biobank adults with baseline Olink plasma GFAP and NfL Incident all-cause dementia / ADRD HRs and prediction AUC for GFAP and NfL Brain multi-omics reveals multimodal AD molecular profiles including a severe cluster.
Integrating transcriptomic/proteomic/metabolomic/lipidomic brain data yielded four multimodal profiles, including Knight-C4 with pronounced dysregulation and worse clinical features.
- How safe is clinic lecanemab in practice?— clinic anti-amyloid treatment experience — not a multi-omics subtype discovery
Study Role Design N Population Outcome Are there molecular subtypes of Alzheimer brains? Supports Computational / modellingMulti-cohort brain multi-omics ML clustering of AD molecular profiles N=42 · Knight-C4 high-dysregulation cluster n=42 within four multimodal profiles Human AD brain cohorts with multi-omic + clinical/neuropath data Multimodal molecular clusters linked to cognition and progression How safe is clinic lecanemab in practice? Qualifiesclinic anti-amyloid treatment experience — not a multi-omics subtype discovery CohortRetrospective consecutive case series of specialty-clinic lecanemab initiations N=234 · Patients with early symptomatic AD receiving ≥1 infusion Early symptomatic Alzheimer disease patients at Washington University Memory Diagnostic Center Infusion reactions, ARIA (including symptomatic), and treatment withdrawal Specialty clinics are delivering lecanemab with real-world workflow constraints.
A specialty memory-clinic report on lecanemab treatment adds practice-level evidence beside biomarker/pathology marker papers.
- Are there molecular subtypes of Alzheimer brains?— molecular subtypes ≠ treatment eligibility/outcomes
Study Role Design N Population Outcome How safe is clinic lecanemab in practice? Supports CohortRetrospective consecutive case series of specialty-clinic lecanemab initiations N=234 · Patients with early symptomatic AD receiving ≥1 infusion Early symptomatic Alzheimer disease patients at Washington University Memory Diagnostic Center Infusion reactions, ARIA (including symptomatic), and treatment withdrawal Are there molecular subtypes of Alzheimer brains? Qualifiesmolecular subtypes ≠ treatment eligibility/outcomes Computational / modellingMulti-cohort brain multi-omics ML clustering of AD molecular profiles N=42 · Knight-C4 high-dysregulation cluster n=42 within four multimodal profiles Human AD brain cohorts with multi-omic + clinical/neuropath data Multimodal molecular clusters linked to cognition and progression A clinic plasma panel plus genetics can discriminate clinical AD from older controls without being autopsy-confirmed diagnosis.
In the AD Cardiff Cohort (1,439 clinical AD cases, 508 older controls), plasma Aβ40/42, P-tau181, NfL, and GFAP plus APOE-ε4 and polygenic risk reached AUC 0.81. Aβ-related peptides were lower in cases; P-tau181, NfL, and GFAP were higher. Case-only GWAS linked the Aβ42/Aβ40 ratio to WWOX and COPG2. Authors note ~25% of clinical AD lack AD pathology at autopsy.
- Blood GFAP and NfL predict dementia years ahead— biobank plasma GFAP/NfL forecast later dementia in volunteers — not same-day clinic discrimination
- Does Alzheimer’s tau hit retinal ganglion cells early?— postmortem retinal tau pathology ≠ plasma Simoa discrimination in living clinic cases
- Is plasma p-tau217 as useful as CSF for Alzheimer PET positivity?— PET amyloid/tau positivity in a memory clinic — not clinical-diagnosis AUC vs older controls
Study Role Design N Population Outcome Can blood markers and genes diagnose Alzheimer’s? Supports Case-controlAD Cardiff Cohort cases vs screened elderly controls; Simoa plasma biomarkers plus GWAS/PRS; clinical diagnosis not CSF/PET-confirmed. N=1947 · 1,439 AD cases (mean age 68) and 508 controls (mean age 82); 1,947 with APOE and genome-wide genotypes. Early- and late-onset sporadic Alzheimer’s disease cases and screened elderly controls from the Alzheimer’s Disease Cardiff Cohort. Discrimination of clinical AD (AUC) by plasma Aβ40/42, P-tau181, NfL, GFAP plus APOE/PRS, and GWAS of biomarkers. Blood GFAP and NfL predict dementia years ahead Qualifiesbiobank plasma GFAP/NfL forecast later dementia in volunteers — not same-day clinic discrimination CohortUK Biobank prospective plasma GFAP/NfL with registry dementia follow-up N=48542 · 1,312 incident all-cause dementia over ~13 years UK Biobank adults with baseline Olink plasma GFAP and NfL Incident all-cause dementia / ADRD HRs and prediction AUC for GFAP and NfL Does Alzheimer’s tau hit retinal ganglion cells early? Qualifiespostmortem retinal tau pathology ≠ plasma Simoa discrimination in living clinic cases Case-controlHuman donor retina/brain comparison of AD dementia, MCI due to AD, and cognitively normal controls N=41 · AD dementia n=15, MCI due to AD n=10, CN controls n=16 Human retinal superior-temporal cross-sections and matched brain donors spanning MCI due to AD, AD dementia, and CN controls Pathogenic tau in RGCs (pS396-tau, oligomeric tau), RGC loss/morphology, and correlations with brain AD pathology and cognition Is plasma p-tau217 as useful as CSF for Alzheimer PET positivity? QualifiesPET amyloid/tau positivity in a memory clinic — not clinical-diagnosis AUC vs older controls Cross-sectionalHead-to-head diagnostic-accuracy study of plasma and CSF p-tau217 vs p-tau181 and p-tau231 against amyloid- and tau-PET in a Geneva memory-clinic cohort. N=114 · 114 participants (CU 33, MCI 67, dementia 14); CSF subset n=36. Memory-clinic patients at Geneva University Hospitals spanning cognitively unimpaired, MCI, and dementia. Correlation with A/T-PET, group effect sizes, and ROC AUC for amyloid- and tau-PET positivity. Pathogenic tau can sit in retinal ganglion cells in MCI and AD, with substantial RGC loss.
In 41 donor eyes, MCI-due-to-AD and AD retinas showed pS396-tau and oligomeric tau inside RGCs, hypertrophic somas and death-pathway markers, about 50% RGC loss, and correlations with brain AD pathology, stage, and cognition.
- How tau buildup shapes brain networks in dementia— in vivo cortical tau PET connectome — not retinal histology
- Can blood markers and genes diagnose Alzheimer’s?— blood protein discrimination in clinic cases — not postmortem RGC counts
Study Role Design N Population Outcome Does Alzheimer’s tau hit retinal ganglion cells early? Supports Case-controlHuman donor retina/brain comparison of AD dementia, MCI due to AD, and cognitively normal controls N=41 · AD dementia n=15, MCI due to AD n=10, CN controls n=16 Human retinal superior-temporal cross-sections and matched brain donors spanning MCI due to AD, AD dementia, and CN controls Pathogenic tau in RGCs (pS396-tau, oligomeric tau), RGC loss/morphology, and correlations with brain AD pathology and cognition How tau buildup shapes brain networks in dementia Qualifiesin vivo cortical tau PET connectome — not retinal histology Case-controlTau PET and functional connectome in Alzheimer's disease vs progressive supranuclear palsy N=34 · 17 AD and 17 PSP Patients with Alzheimer's disease or progressive supranuclear palsy who had capacity to consent Relationship of tau burden to the functional connectome in AD versus PSP Can blood markers and genes diagnose Alzheimer’s? Qualifiesblood protein discrimination in clinic cases — not postmortem RGC counts Case-controlAD Cardiff Cohort cases vs screened elderly controls; Simoa plasma biomarkers plus GWAS/PRS; clinical diagnosis not CSF/PET-confirmed. N=1947 · 1,439 AD cases (mean age 68) and 508 controls (mean age 82); 1,947 with APOE and genome-wide genotypes. Early- and late-onset sporadic Alzheimer’s disease cases and screened elderly controls from the Alzheimer’s Disease Cardiff Cohort. Discrimination of clinical AD (AUC) by plasma Aβ40/42, P-tau181, NfL, GFAP plus APOE/PRS, and GWAS of biomarkers. Plasma p-tau217 can match CSF p-tau217 for PET amyloid/tau status in a memory clinic.
In 114 Geneva memory-clinic patients, plasma p-tau217 identified amyloid/tau PET positivity with mean AUC 0.96, outperforming plasma p-tau181/231 (AUC 0.76/0.79) and similar to CSF p-tau217 (AUC 0.95). CSF n was only 36.
- Can blood markers and genes diagnose Alzheimer’s?— Cardiff clinical AD vs controls with a multi-marker panel — not PET-defined positivity
- Blood GFAP and NfL predict dementia years ahead— UK Biobank GFAP/NfL incident-dementia prognosis — not same-day PET discrimination
Study Role Design N Population Outcome Is plasma p-tau217 as useful as CSF for Alzheimer PET positivity? Supports Cross-sectionalHead-to-head diagnostic-accuracy study of plasma and CSF p-tau217 vs p-tau181 and p-tau231 against amyloid- and tau-PET in a Geneva memory-clinic cohort. N=114 · 114 participants (CU 33, MCI 67, dementia 14); CSF subset n=36. Memory-clinic patients at Geneva University Hospitals spanning cognitively unimpaired, MCI, and dementia. Correlation with A/T-PET, group effect sizes, and ROC AUC for amyloid- and tau-PET positivity. Can blood markers and genes diagnose Alzheimer’s? QualifiesCardiff clinical AD vs controls with a multi-marker panel — not PET-defined positivity Case-controlAD Cardiff Cohort cases vs screened elderly controls; Simoa plasma biomarkers plus GWAS/PRS; clinical diagnosis not CSF/PET-confirmed. N=1947 · 1,439 AD cases (mean age 68) and 508 controls (mean age 82); 1,947 with APOE and genome-wide genotypes. Early- and late-onset sporadic Alzheimer’s disease cases and screened elderly controls from the Alzheimer’s Disease Cardiff Cohort. Discrimination of clinical AD (AUC) by plasma Aβ40/42, P-tau181, NfL, GFAP plus APOE/PRS, and GWAS of biomarkers. Blood GFAP and NfL predict dementia years ahead QualifiesUK Biobank GFAP/NfL incident-dementia prognosis — not same-day PET discrimination CohortUK Biobank prospective plasma GFAP/NfL with registry dementia follow-up N=48542 · 1,312 incident all-cause dementia over ~13 years UK Biobank adults with baseline Olink plasma GFAP and NfL Incident all-cause dementia / ADRD HRs and prediction AUC for GFAP and NfL Nilvadipine did not slow mild-to-moderate Alzheimer disease over 78 weeks.
In 511 people with mild-to-moderate AD, 8 mg nilvadipine daily for 78 weeks was no better than placebo on ADAS-Cog 12 (p=0.465; 9.41 vs 9.63 point decline). CDR-sb and disability scores were also null; adverse events were more common on drug.
- Is plasma p-tau217 as useful as CSF for Alzheimer PET positivity?— biomarker PET accuracy is not a treatment-effect trial
- Do gabapentinoids track with later dementia?— gabapentinoid dementia incidence ≠ calcium-channel-blocker AD treatment RCT
Study Role Design N Population Outcome Does a blood-pressure pill slow Alzheimer decline? Supports RCTPhase III investigator-led double-blind RCT of 8 mg sustained-release nilvadipine vs placebo for 78 weeks across 23 European centres (NILVAD) N=511 · 577 screened; 511 randomised (258 placebo, 253 nilvadipine); mITT n=498 Adults >50 years with mild-to-moderate probable Alzheimer disease (NINCDS-ADRDA; SMMSE 12–26) at 23 academic centres in nine European countries ADAS-Cog 12 progression (primary); gated CDR-sb; function, safety Is plasma p-tau217 as useful as CSF for Alzheimer PET positivity? Qualifiesbiomarker PET accuracy is not a treatment-effect trial Cross-sectionalHead-to-head diagnostic-accuracy study of plasma and CSF p-tau217 vs p-tau181 and p-tau231 against amyloid- and tau-PET in a Geneva memory-clinic cohort. N=114 · 114 participants (CU 33, MCI 67, dementia 14); CSF subset n=36. Memory-clinic patients at Geneva University Hospitals spanning cognitively unimpaired, MCI, and dementia. Correlation with A/T-PET, group effect sizes, and ROC AUC for amyloid- and tau-PET positivity. Do gabapentinoids track with later dementia? Qualifiesgabapentinoid dementia incidence ≠ calcium-channel-blocker AD treatment RCT CohortRetrospective Taiwan NHIRD/LHID 2000–2017 matched cohort of gabapentin or pregabalin users vs 1:5 propensity-matched non-users N=206802 · 34,467 exposed and 172,335 unexposed adults from a 2-million-person 2005 LHID sample Taiwanese adults in the National Health Insurance Research Database who did or did not receive gabapentin or pregabalin Incident dementia (incidence per 100,000 person-years; adjusted HR, including age and cumulative dose strata) Taiwan claims link gabapentin/pregabalin use to higher later dementia rates, especially under age 50.
Among 206,802 matched Taiwanese adults, gabapentin or pregabalin use associated with dementia incidence 980 vs 605 per 100,000 person-years (aHR 1.45), aHR 3.16 under age 50, and a cumulative-dose gradient.
- Does a blood-pressure pill slow Alzheimer decline?— randomized AD treatment null result ≠ observational gabapentinoid exposure risk
- Blood GFAP and NfL predict dementia years ahead— plasma injury-marker prognosis in volunteers — not a drug-exposure claims cohort
Study Role Design N Population Outcome Do gabapentinoids track with later dementia? Supports CohortRetrospective Taiwan NHIRD/LHID 2000–2017 matched cohort of gabapentin or pregabalin users vs 1:5 propensity-matched non-users N=206802 · 34,467 exposed and 172,335 unexposed adults from a 2-million-person 2005 LHID sample Taiwanese adults in the National Health Insurance Research Database who did or did not receive gabapentin or pregabalin Incident dementia (incidence per 100,000 person-years; adjusted HR, including age and cumulative dose strata) Does a blood-pressure pill slow Alzheimer decline? Qualifiesrandomized AD treatment null result ≠ observational gabapentinoid exposure risk RCTPhase III investigator-led double-blind RCT of 8 mg sustained-release nilvadipine vs placebo for 78 weeks across 23 European centres (NILVAD) N=511 · 577 screened; 511 randomised (258 placebo, 253 nilvadipine); mITT n=498 Adults >50 years with mild-to-moderate probable Alzheimer disease (NINCDS-ADRDA; SMMSE 12–26) at 23 academic centres in nine European countries ADAS-Cog 12 progression (primary); gated CDR-sb; function, safety Blood GFAP and NfL predict dementia years ahead Qualifiesplasma injury-marker prognosis in volunteers — not a drug-exposure claims cohort CohortUK Biobank prospective plasma GFAP/NfL with registry dementia follow-up N=48542 · 1,312 incident all-cause dementia over ~13 years UK Biobank adults with baseline Olink plasma GFAP and NfL Incident all-cause dementia / ADRD HRs and prediction AUC for GFAP and NfL
Debates
Tensions and limits
Some items are genuine disagreements on the same question. Others mark different assays, populations, or outcomes.
Plasma GFAP/NfL forecast registry dementia years later in a volunteer cohort; tau/inflammation PET predict short-horizon decline in people already diagnosed with AD. Both can be valid—the limit is not treating prognosis and clinic decline as one assay.
Plasma GFAP/NfL forecast registry dementia years later in a volunteer cohort; tau/inflammation PET predict short-horizon decline in people already diagnosed with AD. Both can be valid—the limit is not treating prognosis and clinic decline as one assay.
- Blood GFAP and NfL predict dementia years ahead
- Using Brain Scans to Predict Cognitive Decline in Alzheimer's
Study Role Design N Population Outcome Blood GFAP and NfL predict dementia years ahead Supports CohortUK Biobank prospective plasma GFAP/NfL with registry dementia follow-up N=48542 · 1,312 incident all-cause dementia over ~13 years UK Biobank adults with baseline Olink plasma GFAP and NfL Incident all-cause dementia / ADRD HRs and prediction AUC for GFAP and NfL Using Brain Scans to Predict Cognitive Decline in Alzheimer's Supports CohortBaseline MRI/PET (tau, microglial activation, atrophy) predicting 3-year cognitive decline N=55 · 26 Alzheimer’s-pathology patients (12 dementia, 14 amnestic MCI) and 29 healthy controls Patients with Alzheimer’s pathology and healthy controls with longitudinal cognition Baseline tau and microglial activation predicting decline; atrophy adding no independent value
PaperFren reads this as a limit on how far one study travels — different assays, populations, or outcomes — not a forced fight between papers.
VR navigation separates biomarker-defined MCI behaviourally; CSF tau in unimpaired adults tracks hippocampal hyperactivity and object memory. Shared theme: early Alzheimer’s biology can show up before frank dementia—different tasks, samples, and endpoints.
VR navigation separates biomarker-defined MCI behaviourally; CSF tau in unimpaired adults tracks hippocampal hyperactivity and object memory. Shared theme: early Alzheimer’s biology can show up before frank dementia—different tasks, samples, and endpoints.
- Using Virtual Reality to Detect Early Alzheimer's Disease
- Does brain tau protein affect object memory in older adults?
Study Role Design N Population Outcome Using Virtual Reality to Detect Early Alzheimer's Disease Supports Cross-sectionalImmersive VR navigation test comparing biomarker-defined MCI patients and healthy controls N=86 · 45 MCI patients (12 biomarker-positive, 14 biomarker-negative among CSF-tested) and 41 healthy controls Mild cognitive impairment patients and healthy controls performing entorhinal-based VR navigation Navigation error distinguishing biomarker-positive early Alzheimer’s MCI from biomarker-negative MCI and controls Does brain tau protein affect object memory in older adults? Supports OtherObservational CSF biomarker–fMRI association study; no assigned exposure N=21 · 21 cognitively unimpaired older adults analysed after spinal tap and mnemonic discrimination fMRI Cognitively unimpaired older adults Object mnemonic discrimination and hippocampal activation vs CSF tau
PaperFren reads this as a limit on how far one study travels — different assays, populations, or outcomes — not a forced fight between papers.
Clinic plasma+genetics discrimination, biobank GFAP/NfL prognosis, cortical tau PET, and postmortem retinal tau are related Alzheimer’s biology at different compartments, time horizons, and confirmation standards. They do not yield one interchangeable “accuracy number.”
Clinic plasma+genetics discrimination, biobank GFAP/NfL prognosis, cortical tau PET, and postmortem retinal tau are related Alzheimer’s biology at different compartments, time horizons, and confirmation standards. They do not yield one interchangeable “accuracy number.”
- Can blood markers and genes diagnose Alzheimer’s?
- Blood GFAP and NfL predict dementia years ahead
- Does Alzheimer’s tau hit retinal ganglion cells early?
Study Role Design N Population Outcome Can blood markers and genes diagnose Alzheimer’s? Supports Case-controlAD Cardiff Cohort cases vs screened elderly controls; Simoa plasma biomarkers plus GWAS/PRS; clinical diagnosis not CSF/PET-confirmed. N=1947 · 1,439 AD cases (mean age 68) and 508 controls (mean age 82); 1,947 with APOE and genome-wide genotypes. Early- and late-onset sporadic Alzheimer’s disease cases and screened elderly controls from the Alzheimer’s Disease Cardiff Cohort. Discrimination of clinical AD (AUC) by plasma Aβ40/42, P-tau181, NfL, GFAP plus APOE/PRS, and GWAS of biomarkers. Blood GFAP and NfL predict dementia years ahead Supports CohortUK Biobank prospective plasma GFAP/NfL with registry dementia follow-up N=48542 · 1,312 incident all-cause dementia over ~13 years UK Biobank adults with baseline Olink plasma GFAP and NfL Incident all-cause dementia / ADRD HRs and prediction AUC for GFAP and NfL Does Alzheimer’s tau hit retinal ganglion cells early? Supports Case-controlHuman donor retina/brain comparison of AD dementia, MCI due to AD, and cognitively normal controls N=41 · AD dementia n=15, MCI due to AD n=10, CN controls n=16 Human retinal superior-temporal cross-sections and matched brain donors spanning MCI due to AD, AD dementia, and CN controls Pathogenic tau in RGCs (pS396-tau, oligomeric tau), RGC loss/morphology, and correlations with brain AD pathology and cognition
PaperFren reads this as a limit on how far one study travels — different assays, populations, or outcomes — not a forced fight between papers.
PET-confirmed p-tau217 accuracy, a null nilvadipine AD RCT, and gabapentinoid dementia incidence answer different questions. A high diagnostic AUC does not imply a drug will slow ADAS-Cog, and claims associations are not trial evidence.
PET-confirmed p-tau217 accuracy, a null nilvadipine AD RCT, and gabapentinoid dementia incidence answer different questions. A high diagnostic AUC does not imply a drug will slow ADAS-Cog, and claims associations are not trial evidence.
- Is plasma p-tau217 as useful as CSF for Alzheimer PET positivity?
- Does a blood-pressure pill slow Alzheimer decline?
- Do gabapentinoids track with later dementia?
Study Role Design N Population Outcome Is plasma p-tau217 as useful as CSF for Alzheimer PET positivity? Supports Cross-sectionalHead-to-head diagnostic-accuracy study of plasma and CSF p-tau217 vs p-tau181 and p-tau231 against amyloid- and tau-PET in a Geneva memory-clinic cohort. N=114 · 114 participants (CU 33, MCI 67, dementia 14); CSF subset n=36. Memory-clinic patients at Geneva University Hospitals spanning cognitively unimpaired, MCI, and dementia. Correlation with A/T-PET, group effect sizes, and ROC AUC for amyloid- and tau-PET positivity. Does a blood-pressure pill slow Alzheimer decline? Supports RCTPhase III investigator-led double-blind RCT of 8 mg sustained-release nilvadipine vs placebo for 78 weeks across 23 European centres (NILVAD) N=511 · 577 screened; 511 randomised (258 placebo, 253 nilvadipine); mITT n=498 Adults >50 years with mild-to-moderate probable Alzheimer disease (NINCDS-ADRDA; SMMSE 12–26) at 23 academic centres in nine European countries ADAS-Cog 12 progression (primary); gated CDR-sb; function, safety Do gabapentinoids track with later dementia? Supports CohortRetrospective Taiwan NHIRD/LHID 2000–2017 matched cohort of gabapentin or pregabalin users vs 1:5 propensity-matched non-users N=206802 · 34,467 exposed and 172,335 unexposed adults from a 2-million-person 2005 LHID sample Taiwanese adults in the National Health Insurance Research Database who did or did not receive gabapentin or pregabalin Incident dementia (incidence per 100,000 person-years; adjusted HR, including age and cumulative dose strata)
PaperFren reads this as a limit on how far one study travels — different assays, populations, or outcomes — not a forced fight between papers.
Timeline
How understanding moved
Study years are when the paper was published. Evidence edits are dated changes to this page's claims. Explanations are when PaperFren added a Discovery — not a claim that the science happened that day.
2026
- Added a scope qualifier
How safe is clinic lecanemab in practice?
- Added a scope qualifier
Are there molecular subtypes of Alzheimer brains?
- Added a supporting study
Are there molecular subtypes of Alzheimer brains?
- Added a supporting study
How safe is clinic lecanemab in practice?
Concept page published
Alzheimer’s and MCI markers
New claim
Integrating transcriptomic/proteomic/metabolomic/lipidomic brain data yielded four multimodal profiles, including Knight-C4 with pronounced dysregulation and worse clinical features.
New claim
A specialty memory-clinic report on lecanemab treatment adds practice-level evidence beside biomarker/pathology marker papers.
- Added a scope qualifier
How safe is clinic lecanemab in practice?
- Added a scope qualifier
Are there molecular subtypes of Alzheimer brains?
- Added a supporting study
Are there molecular subtypes of Alzheimer brains?
- Added a supporting study
How safe is clinic lecanemab in practice?
New claim
Integrating transcriptomic/proteomic/metabolomic/lipidomic brain data yielded four multimodal profiles, including Knight-C4 with pronounced dysregulation and worse clinical features.
New claim
A specialty memory-clinic report on lecanemab treatment adds practice-level evidence beside biomarker/pathology marker papers.
Added a misconception
A plasma AD panel with AUC 0.81 can replace CSF/PET or autopsy for diagnosis.
Added a misconception
Tau-laden retinal ganglion cells already amount to an in-clinic eye-scan biomarker.
Added a misconception
Plasma p-tau217 AUC 0.96 means a blood test can replace PET everywhere.
- Added a scope qualifier
Can blood markers and genes diagnose Alzheimer’s?
- Added a scope qualifier
Does Alzheimer’s tau hit retinal ganglion cells early?
- Added a scope qualifier
Blood GFAP and NfL predict dementia years ahead
- Added a scope qualifier
Does Alzheimer’s tau hit retinal ganglion cells early?
- Added a scope qualifier
Can blood markers and genes diagnose Alzheimer’s?
- Added a scope qualifier
How tau buildup shapes brain networks in dementia
- Added a scope qualifier
Is plasma p-tau217 as useful as CSF for Alzheimer PET positivity?
- Added a scope qualifier
Blood GFAP and NfL predict dementia years ahead
- Added a scope qualifier
Can blood markers and genes diagnose Alzheimer’s?
- Added a scope qualifier
Is plasma p-tau217 as useful as CSF for Alzheimer PET positivity?
- Added a scope qualifier
Do gabapentinoids track with later dementia?
- Added a scope qualifier
Blood GFAP and NfL predict dementia years ahead
- Added a scope qualifier
Does a blood-pressure pill slow Alzheimer decline?
- Added a supporting study
Can blood markers and genes diagnose Alzheimer’s?
- Added a supporting study
Does Alzheimer’s tau hit retinal ganglion cells early?
- Added a supporting study
Blood GFAP and NfL predict dementia years ahead
- Added a supporting study
Can blood markers and genes diagnose Alzheimer’s?
- Added a supporting study
Does Alzheimer’s tau hit retinal ganglion cells early?
- Added a supporting study
Is plasma p-tau217 as useful as CSF for Alzheimer PET positivity?
- Added a supporting study
Does a blood-pressure pill slow Alzheimer decline?
- Added a supporting study
Do gabapentinoids track with later dementia?
- Added a supporting study
Is plasma p-tau217 as useful as CSF for Alzheimer PET positivity?
- Added a supporting study
Does a blood-pressure pill slow Alzheimer decline?
- Added a supporting study
Do gabapentinoids track with later dementia?
New claim
In the AD Cardiff Cohort (1,439 clinical AD cases, 508 older controls), plasma Aβ40/42, P-tau181, NfL, and GFAP plus APOE-ε4 and polygenic risk reached AUC 0.81. Aβ-related peptides were lower in cases; P-tau181, NfL, and GFAP were higher. Case-only GWAS linked the Aβ42/Aβ40 ratio to WWOX and COPG2. Authors note ~25% of clinical AD lack AD pathology at autopsy.
New claim
In 41 donor eyes, MCI-due-to-AD and AD retinas showed pS396-tau and oligomeric tau inside RGCs, hypertrophic somas and death-pathway markers, about 50% RGC loss, and correlations with brain AD pathology, stage, and cognition.
New claim
In 114 Geneva memory-clinic patients, plasma p-tau217 identified amyloid/tau PET positivity with mean AUC 0.96, outperforming plasma p-tau181/231 (AUC 0.76/0.79) and similar to CSF p-tau217 (AUC 0.95). CSF n was only 36.
New claim
In 511 people with mild-to-moderate AD, 8 mg nilvadipine daily for 78 weeks was no better than placebo on ADAS-Cog 12 (p=0.465; 9.41 vs 9.63 point decline). CDR-sb and disability scores were also null; adverse events were more common on drug.
New claim
Among 206,802 matched Taiwanese adults, gabapentin or pregabalin use associated with dementia incidence 980 vs 605 per 100,000 person-years (aHR 1.45), aHR 3.16 under age 50, and a cumulative-dose gradient.
New tension
Clinic plasma+genetics discrimination, biobank GFAP/NfL prognosis, cortical tau PET, and postmortem retinal tau are related Alzheimer’s biology at different compartments, time horizons, and confirmation standards. They do not yield one interchangeable “accuracy number.”
New tension
PET-confirmed p-tau217 accuracy, a null nilvadipine AD RCT, and gabapentinoid dementia incidence answer different questions. A high diagnostic AUC does not imply a drug will slow ADAS-Cog, and claims associations are not trial evidence.
Change log
What changed
Dated edits to this page's evidence: studies added or removed from a claim, claims added or withdrawn, and new explanations tagged here. Coverage edits are distinct from reviewed research changes and corrections. Dates record PaperFren updates; study publication dates appear in the timeline.
In UK Biobank adults with baseline plasma measures, higher GFAP and NfL associated with roughly doubled hazards of incident all-cause dementia over ~13 years, with elevations detectable up to about 15 years before diagnosis and incremental prediction beyond demographic risk scores.
- Coverage updated · Added a scope qualifier: Can blood markers and genes diagnose Alzheimer’s?
In Alzheimer’s disease, tau PET burden concentrated in highly connected cortical hubs and higher overall tau associated with weakened cortical connection strength; progressive-supranuclear-palsy patterns differed, showing disease-specific mapping of tau onto networks.
- Coverage updated · Added a scope qualifier: Does Alzheimer’s tau hit retinal ganglion cells early?
In the AD Cardiff Cohort (1,439 clinical AD cases, 508 older controls), plasma Aβ40/42, P-tau181, NfL, and GFAP plus APOE-ε4 and polygenic risk reached AUC 0.81. Aβ-related peptides were lower in cases; P-tau181, NfL, and GFAP were higher. Case-only GWAS linked the Aβ42/Aβ40 ratio to WWOX and COPG2. Authors note ~25% of clinical AD lack AD pathology at autopsy.
- Coverage updated · New claim
- Coverage updated · Added a supporting study: Can blood markers and genes diagnose Alzheimer’s?
- Coverage updated · Added a scope qualifier: Blood GFAP and NfL predict dementia years ahead
- Coverage updated · Added a scope qualifier: Does Alzheimer’s tau hit retinal ganglion cells early?
In 41 donor eyes, MCI-due-to-AD and AD retinas showed pS396-tau and oligomeric tau inside RGCs, hypertrophic somas and death-pathway markers, about 50% RGC loss, and correlations with brain AD pathology, stage, and cognition.
- Coverage updated · New claim
- Coverage updated · Added a supporting study: Does Alzheimer’s tau hit retinal ganglion cells early?
- Coverage updated · Added a scope qualifier: Can blood markers and genes diagnose Alzheimer’s?
- Coverage updated · Added a scope qualifier: How tau buildup shapes brain networks in dementia
Clinic plasma+genetics discrimination, biobank GFAP/NfL prognosis, cortical tau PET, and postmortem retinal tau are related Alzheimer’s biology at different compartments, time horizons, and confirmation standards. They do not yield one interchangeable “accuracy number.”
- Coverage updated · New tension
- Coverage updated · Added a supporting study: Blood GFAP and NfL predict dementia years ahead
- Coverage updated · Added a supporting study: Can blood markers and genes diagnose Alzheimer’s?
- Coverage updated · Added a supporting study: Does Alzheimer’s tau hit retinal ganglion cells early?
A plasma AD panel with AUC 0.81 can replace CSF/PET or autopsy for diagnosis.
- Coverage updated · Added a misconception
Tau-laden retinal ganglion cells already amount to an in-clinic eye-scan biomarker.
- Coverage updated · Added a misconception
In the AD Cardiff Cohort (1,439 clinical AD cases, 508 older controls), plasma Aβ40/42, P-tau181, NfL, and GFAP plus APOE-ε4 and polygenic risk reached AUC 0.81. Aβ-related peptides were lower in cases; P-tau181, NfL, and GFAP were higher. Case-only GWAS linked the Aβ42/Aβ40 ratio to WWOX and COPG2. Authors note ~25% of clinical AD lack AD pathology at autopsy.
- Coverage updated · Added a scope qualifier: Is plasma p-tau217 as useful as CSF for Alzheimer PET positivity?
In 114 Geneva memory-clinic patients, plasma p-tau217 identified amyloid/tau PET positivity with mean AUC 0.96, outperforming plasma p-tau181/231 (AUC 0.76/0.79) and similar to CSF p-tau217 (AUC 0.95). CSF n was only 36.
- Coverage updated · New claim
- Coverage updated · Added a supporting study: Is plasma p-tau217 as useful as CSF for Alzheimer PET positivity?
- Coverage updated · Added a scope qualifier: Blood GFAP and NfL predict dementia years ahead
- Coverage updated · Added a scope qualifier: Can blood markers and genes diagnose Alzheimer’s?
In 511 people with mild-to-moderate AD, 8 mg nilvadipine daily for 78 weeks was no better than placebo on ADAS-Cog 12 (p=0.465; 9.41 vs 9.63 point decline). CDR-sb and disability scores were also null; adverse events were more common on drug.
- Coverage updated · New claim
- Coverage updated · Added a supporting study: Does a blood-pressure pill slow Alzheimer decline?
- Coverage updated · Added a scope qualifier: Is plasma p-tau217 as useful as CSF for Alzheimer PET positivity?
- Coverage updated · Added a scope qualifier: Do gabapentinoids track with later dementia?
Among 206,802 matched Taiwanese adults, gabapentin or pregabalin use associated with dementia incidence 980 vs 605 per 100,000 person-years (aHR 1.45), aHR 3.16 under age 50, and a cumulative-dose gradient.
- Coverage updated · New claim
- Coverage updated · Added a supporting study: Do gabapentinoids track with later dementia?
- Coverage updated · Added a scope qualifier: Blood GFAP and NfL predict dementia years ahead
- Coverage updated · Added a scope qualifier: Does a blood-pressure pill slow Alzheimer decline?
PET-confirmed p-tau217 accuracy, a null nilvadipine AD RCT, and gabapentinoid dementia incidence answer different questions. A high diagnostic AUC does not imply a drug will slow ADAS-Cog, and claims associations are not trial evidence.
- Coverage updated · New tension
- Coverage updated · Added a supporting study: Is plasma p-tau217 as useful as CSF for Alzheimer PET positivity?
- Coverage updated · Added a supporting study: Does a blood-pressure pill slow Alzheimer decline?
- Coverage updated · Added a supporting study: Do gabapentinoids track with later dementia?
Show 6 earlierShow fewer
Plasma p-tau217 AUC 0.96 means a blood test can replace PET everywhere.
- Coverage updated · Added a misconception
Integrating transcriptomic/proteomic/metabolomic/lipidomic brain data yielded four multimodal profiles, including Knight-C4 with pronounced dysregulation and worse clinical features.
- Coverage updated · New claim
- Coverage updated · Added a supporting study: Are there molecular subtypes of Alzheimer brains?
- Coverage updated · Added a scope qualifier: How safe is clinic lecanemab in practice?
A specialty memory-clinic report on lecanemab treatment adds practice-level evidence beside biomarker/pathology marker papers.
- Coverage updated · New claim
- Coverage updated · Added a supporting study: How safe is clinic lecanemab in practice?
- Coverage updated · Added a scope qualifier: Are there molecular subtypes of Alzheimer brains?
- Coverage updated · Concept page published
Integrating transcriptomic/proteomic/metabolomic/lipidomic brain data yielded four multimodal profiles, including Knight-C4 with pronounced dysregulation and worse clinical features.
- Coverage updated · New claim
- Coverage updated · Added a supporting study: Are there molecular subtypes of Alzheimer brains?
- Coverage updated · Added a scope qualifier: How safe is clinic lecanemab in practice?
A specialty memory-clinic report on lecanemab treatment adds practice-level evidence beside biomarker/pathology marker papers.
- Coverage updated · New claim
- Coverage updated · Added a supporting study: How safe is clinic lecanemab in practice?
- Coverage updated · Added a scope qualifier: Are there molecular subtypes of Alzheimer brains?
Papers
12 studies in this library bear on Alzheimer’s and MCI markers, ordered by citations.
- How tau buildup shapes brain networks in dementia
In Alzheimer's disease, tau builds up in highly connected brain hubs and weakens their connections, while in progressive supranuclear palsy, tau accumulates in deep brain structures and forces the cortex to use less efficient, indirect pathways.
- Using Brain Scans to Predict Cognitive Decline in Alzheimer's
Baseline PET scans tracking tau protein and brain inflammation predict future cognitive decline over three years, while brain shrinkage measurements add no extra predictive power.
- Using Virtual Reality to Detect Early Alzheimer's Disease
A virtual reality walking test assessing entorhinal cortex function accurately identifies patients with early-stage, biomarker-proven Alzheimer's disease.
- Can blood markers and genes diagnose Alzheimer’s?
In 1,439 AD cases and 508 older controls, combining plasma Aβ40/42, P-tau181, NfL, GFAP with APOE and PRS reached AUC 0.81; case-only GWAS linked Aβ42/Aβ40 to WWOX and COPG2.
- Does a blood-pressure pill slow Alzheimer decline?
In 511 people with mild-to-moderate Alzheimer disease, 8 mg nilvadipine daily for 78 weeks was safe but no better than placebo on ADAS-Cog 12 (p=0.465).
- Blood GFAP and NfL predict dementia years ahead
In 48,542 UK Biobank participants followed ~13 years, elevated plasma GFAP and NfL preceded dementia up to 15 years and improved prediction beyond CAIDE/DRS risk scores (AUC up to ~0.89).
- Is plasma p-tau217 as useful as CSF for Alzheimer PET positivity?
In 114 Geneva memory-clinic patients, plasma p-tau217 identified amyloid/tau PET positivity (mean AUC 0.96) better than p-tau181/231 and similarly to CSF p-tau217 (AUC 0.95).
- Does brain tau protein affect object memory in older adults?
Elevated levels of tau protein in the brain fluid of healthy older adults are linked to overactivity in the hippocampus and worse memory for distinguishing highly similar objects.
Show 4 more studiesShow fewer studies
- How safe is clinic lecanemab in practice?
Among 234 memory-clinic patients on lecanemab, infusion reactions (37%) and ARIA (22%) were common but generally manageable; mild dementia had much higher symptomatic ARIA.
- Are there molecular subtypes of Alzheimer brains?
Brain multi-omics integration found four multimodal AD profiles, including severe Knight-C4 with worse cognition and heavy molecular dysregulation.
- Does Alzheimer’s tau hit retinal ganglion cells early?
In 41 donor eyes, MCI and AD retinas showed pS396-tau and oligomeric tau inside RGCs, ~50% ganglion-cell loss, and correlations with brain AD stage and cognition.
- Do gabapentinoids track with later dementia?
Among 206,802 Taiwanese adults, gabapentin or pregabalin use was linked to higher dementia incidence (980 vs 605 per 100,000 person-years; aHR 1.45), with aHR 3.16 under age 50 and a cumulative-dose gradient.
Compare studies
Select 2–10 studies. Design and N are labels, not a ranking.
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Questions
What is still open
Plasma GFAP/NfL forecast registry dementia years later in a volunteer cohort; tau/inflammation PET predict short-horizon decline in people already diagnosed with AD. Both can be valid—the limit is not treating prognosis and clinic decline as one assay.
VR navigation separates biomarker-defined MCI behaviourally; CSF tau in unimpaired adults tracks hippocampal hyperactivity and object memory. Shared theme: early Alzheimer’s biology can show up before frank dementia—different tasks, samples, and endpoints.
Clinic plasma+genetics discrimination, biobank GFAP/NfL prognosis, cortical tau PET, and postmortem retinal tau are related Alzheimer’s biology at different compartments, time horizons, and confirmation standards. They do not yield one interchangeable “accuracy number.”
PET-confirmed p-tau217 accuracy, a null nilvadipine AD RCT, and gabapentinoid dementia incidence answer different questions. A high diagnostic AUC does not imply a drug will slow ADAS-Cog, and claims associations are not trial evidence.
Ask PaperFren about Alzheimer’s and MCI markers
Study this conceptflashcards and short-answer questions
Why can plasma NfL/GFAP prognosis and tau PET decline prediction both be true without being the same claim?
They answer different questions in different populations: biobank adults years before dementia versus people already diagnosed with AD over a few years. Shared biology (neurodegeneration signals) does not make the assays interchangeable.
A clinic wants one “Alzheimer’s accuracy number” pooling VR MCI discrimination with biobank AUCs. What goes wrong?
Those metrics come from different outcomes (task error vs incident dementia), prevalences, and time horizons. Pooling invents a head-to-head that the designs do not support.
How should you compare a clinic plasma AUC with UK Biobank GFAP/NfL hazard ratios?
They answer different questions: same-day discrimination of clinical AD vs controls versus years-ahead incident dementia in volunteers. Different outcomes, prevalences, and time horizons block a pooled accuracy claim.
Why doesn’t a null nilvadipine AD trial contradict a high plasma p-tau217 AUC?
One tests whether a calcium-channel blocker changes cognition over 78 weeks; the other tests whether a blood protein matches PET amyloid/tau status. Different questions, populations, and endpoints.
Flashcards
0 of 8 answers reviewed