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 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.

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.

The result points two ways: p-tau181 gave the best AUC for separating AD from controls, frontotemporal dementia and amyloid-negative Lewy body dementia, but that discrimination could not be reproduced when pre-defined cut-offs were applied, so cohort-specific cut-offs were needed.

Direction is for the test's accuracy against the reference standard; an accuracy result, not a health outcome. Serum GFAP tracked post-mortem tau pathology independently of amyloid, correlated negatively with brain weight and cognition, correlated with astrocyte reactivity in tissue, and separated neuropathologically confirmed AD from non-AD dementias with AUC 0.91.

Direction is for higher baseline plasma GFAP: it detected abnormal CSF amyloid (AUC 0.79, 0.86 with APOE4) and predicted later conversion to Alzheimer's dementia (AUC 0.84); GFAP slopes were steeper in those who progressed.

Direction is for the test's accuracy against the reference standard; an accuracy result, not a health outcome. Results ranged from 55% to 100% sensitivity and 60% to 100% specificity across four laboratories using different protocols, with only fair agreement between them (kappa 0.246).

Direction is for the test's accuracy against the reference standard; an accuracy result, not a health outcome. Smell testing followed by CSF seed amplification only in those with reduced smell predicted brain Lewy body pathology with 94% accuracy and cut CSF testing by 43%; in a living cohort it predicted CSF assay status with 79% accuracy.

A pooled prevalence among carers (50.8% lonely, 37.1% socially isolated) with no non-carer comparison, so no direction for the effect of caregiving can be recorded.

No significant difference in 5-year cumulative spending between spouses of people with and without dementia ($3,974, 95% CI -$3,199 to $11,477); year-5 spending was higher (+$2,748), driven by inpatient costs.

Direction is for BEING a carer: carers were worse off than non-carers on every domain, with the largest gaps in depression and stress.

Only STRAINED carers were at higher risk (RR 1.63, 95% CI 1.00-2.65, with the interval touching 1). Carers who reported no strain showed nothing (RR 1.08), so it is the strain rather than the caregiving that carries the signal.

Benefit was larger for younger, male and non-spousal carers. The largest single effect (training the person with dementia) rests on 10 observations and the authors call it promising rather than definitive.

A pilot designed to test feasibility; 68 carers and a 2-week outcome.

Digital psychological interventions reduced caregiver burden and improved self-efficacy and quality of life; the effect on depressive symptoms was not statistically significant (P = .06).

No difference from waitlist control on the primary burden outcome or on mood, WHOQOL-Bref or productivity; only the CarerQoL-VAS quality-of-life score was higher in the intervention group. The trial recruited 93 of a 194 target.

At the 1-month comparison the automated self-guided programme reduced depression and burden and increased positive gains versus waitlist; anxiety did not differ. Group differences mostly disappeared once controls received the programme.

Peer support reduced distress to behavioural symptoms and increased social support and quality of life immediately after the intervention, but had no effect on depression/anxiety, loneliness, burden or competence, and no outcome was sustained at follow-up.

A factorial trial of components: the mindfulness component carried the benefit and amplified the others.

Burden fell in both arms with no significant difference between the two platforms. There was no untreated control, so the within-arm improvement cannot be separated from time or attention.

Direction is for NIDUS-Family: an 89% probability of cost-effectiveness from a health and social care perspective (87% societal) and £8,934 (37%) lower average costs, though the cost difference's confidence interval includes zero.

The outcome is how prepared carers felt to decide about firearm access, not whether any injury was avoided.

Direction is for psychosocial and pharmacological interventions, which the review reports as showing mild to modest efficacy in high-quality meta-analyses. A narrative clinical review summarising other meta-analyses, not a new pooled estimate.

Benefit in Hispanic and White caregivers and in Black spousal caregivers; not in Black non-spousal caregivers.

Direction is for the test's accuracy against the reference standard; an accuracy result, not a health outcome. Tablet tests correlated strongly with MMSE, MoCA and Trails A (r > 0.7) and the Match test separated amyloid-positive from -negative patients (AUC 0.82) better than MMSE or MoCA (0.75).

Direction is for the test's accuracy against the reference standard; an accuracy result, not a health outcome. Pooled sensitivity 76% and specificity 83% for dementia, with 73% / 84% in primary care; the authors call it a practical screening tool while noting high or unclear risk of bias in patient selection and timing.

Direction is for the test's accuracy against the reference standard; an accuracy result, not a health outcome. The two-stage GPCOG had sensitivity 0.85 and specificity 0.86 against DSM-IV dementia, and was superior to the Abbreviated Mental Test.

A cost estimate ($818 billion, 80% of it borne by families through unpaid care, earnings losses, out-of-pocket costs and quality-of-life losses) with no exposure compared, so no direction is recorded.

A descriptive spending analysis with no exposure compared, so there is no direction to record: Part D spending rose with dual-eligibility duration, Part B drug spending varied widely by state, and ACO enrollment made only a modest difference.

Direction is for having AD dementia: lifetime formal-care costs of 2,440,000 SEK against 510,000 SEK for matched controls, with prescriptions and social care rising and specialist outpatient visits falling as the disease advanced. A cost result, not a health outcome.

A cost projection: total burden is estimated at $344 billion in 2020 rising to over $3 trillion in 2060, with African American and Latino families projected to bear a disproportionate share. It compares spending shares between groups but tests no exposure, so no direction is recorded.

A cost estimate with no exposure compared, so there is no direction to record. Higher unpaid-care costs went with lower medical spending on nursing facility care.

A cost projection with no exposure compared, so there is no direction to record. Dementia's share of replacement cost is projected to rise from 44% to 53%.

A cost estimate with no exposure compared, so there is no direction to record.

Direction is for greater disease severity: mean annual costs rose from SEK 99,906 in MCI to SEK 795,617 in severe AD (SEK 57,625 to 668,073 in the amyloid-confirmed subset), driven by institutionalisation, home care and daytime support while outpatient costs fell. A cost result, not a health outcome.

Direction is for being on the Alzheimer's continuum: societal costs were 52% higher in subjective cognitive decline, 170% in MCI and 307% in AD dementia than in controls, and payer costs 26%, 85% and 36% higher. A cost result, not a health outcome.

A cost estimate and projection with no exposure compared, so there is no direction to record.

A cost estimation across 204 countries with no exposure compared, so there is no direction to record.

Direction is for being non-Hispanic Black or Hispanic rather than non-Hispanic White: disease-course Medicare spending was higher ($165,730 and $160,442 versus $136,326), highest for Black beneficiaries in every phase and driven by high-cost services in the last year of life. A disparities result, not a biological effect of race.

Direction is for dying with dementia rather than heart disease, cancer or other causes: total cost was higher ($287,038) and out-of-pocket spending 81% higher, consuming 32% of household wealth versus 11%.

Direction is for living in the community rather than a nursing home: unadjusted costs were lower in the community, but after adjusting for functional impairment and comorbidity community care cost €11,344 more per year, mainly through informal care. A cost result, not a health outcome.

Direction is for having dementia: the attributable yearly cost per person was $41,689-$56,290 depending on how informal care is valued, a burden the authors call similar to heart disease and cancer.

Direction is for value for money at current Australian prices: donanemab improved modelled QALYs (4.38 vs 4.01) but the ICER of $342,424 per QALY exceeded commonly cited willingness-to-pay thresholds. An unfavourable value result, not a clinical harm.

A threshold analysis estimating what each country should be willing to pay (from $4-$18 a year in low-income countries to $254-$9,434 for lecanemab and $387-$13,964 for donanemab in high-income countries). It sets no price against an actual list price, so there is no direction to record.

The review splits by drug class: at $100,000 per QALY every study found memantine cost-effective and more than half found the cholinesterase inhibitors so, whereas aducanumab, lecanemab and donanemab were not cost-effective in any study. A value result, not a clinical harm.

A cost-effectiveness model reporting ICERs of JPY 8.5 million and 7.9 million per QALY without stating a threshold or a verdict; the authors argue that narrow value assessments understate social value. No direction is recorded.

Direction is for value for money: three years of lecanemab gained 0.17 QALYs and the cost-effective price at 1 million SEK per QALY was 33,886 SEK a year, which the authors say makes it unlikely to be cost effective in Sweden at current US list prices. An unfavourable value result, not a clinical harm.

Direction is for value for money at the current price: no lecanemab strategy was cost-effective against standard care alone, whichever diagnostic test was used; CSF-guided targeted treatment would become cost-effective below $5,100 per year. An unfavourable value result, not a clinical harm.

Direction is for chronic bi-weekly intravenous infusion relative to oral treatment: administration and monitoring cost $45,208 plus $6,095 caregiver burden, eroding 44% of treatment value, against 2% for an oral drug. A cost result for a hypothetical treatment, not a clinical harm.

Direction is for value for money at the list price: the benchmark price ($8,900-$21,500 per year) sits below the $26,500 list price, the committee voted 15-0 that the drug represents low long-term value at that price and 12-3 that the evidence did not adequately demonstrate a net health benefit. An unfavourable value assessment, not a clinical harm.

Direction is for value for money at the assumed $28,000 annual price: ICERs of $981,000/QALY (aducanumab) and $193,000/QALY (donanemab) exceed the $150,000/QALY threshold, so neither was cost-effective. An unfavourable value result, not a clinical harm.

The community health worker programme achieved verified linkage to medical care in 16.7% of dyads versus none in the control arm. Caregiver outcomes were largely unchanged, with self-efficacy favouring control.

No difference between health-system care, community-based care or usual care on either primary outcome. Caregiver self-efficacy did improve in both active arms.

Direction is for the extended nursing role intervention: 74% fewer unmet needs and higher quality of life at six months, with a small QALY gain at about 1,425 EUR added cost; no effect on caregiver burden.

The two perspectives disagree: the digitally supported care management system dominated usual care for the public payer (lower costs, marginally more QALYs, 72-79% probability of cost-effectiveness) but cost €331,000 per QALY from a societal perspective (33-35% probability).

Direction is for the Care Ecosystem programme: total cost of care was $475.80 per member per month lower than matched controls at 12 months, with fewer emergency, outpatient and professional visits.

Direction is for collaborative dementia care management: fewer neuropsychiatric symptoms, lower caregiver burden, better mental health and 0.137 QALYs gained at no significant added cost (3186€ per QALY) over 36 months; no difference in antidementia drug use, overall quality of life or inappropriate medication.

No benefit and no harm: screening did not change family-member quality of life, preparedness or self-efficacy, and did not raise depression or anxiety. Only 5.1% screened positive.

The outcome is how many diagnoses were made, not whether anyone was better off. The passive digital marker alone did not raise detection (AOR 0.84, 95% CI 0.63-1.11).

MCI was diagnosed sooner (HR 1.21) but dementia diagnosis barely moved (HR 1.04, 95% CI 1.02-1.06). The outcome is detection, not health.

A criteria document. It defines Alzheimer's disease biologically and sets out staging, and reports no effect estimate.

An editorial. It argues that biomarker positivity alone should not define Alzheimer's disease in people without symptoms, and reports no data of its own.

A research framework defining Alzheimer's disease by biomarkers (the AT(N) system) for research use. It states its own intended limits and reports no effect estimate.

Consensus guidance for primary care on disclosing and communicating a dementia diagnosis, developed with patients, care partners and clinicians. It reports no effect estimate.

A clinical practice guideline. It sets out a structured, patient-centred process for evaluating, diagnosing and disclosing suspected Alzheimer's disease or related dementias in any practice setting, and reports no effect estimate.

Direction is for a lower (worse) glymphatic index: it was lowest in AD dementia and predicted faster amyloid accumulation, amyloid-positive transition, atrophy, clinical progression and cognitive decline, with the cognitive effect fully mediated by amyloid PET and atrophy.

Difference-in-differences around ACO entry found no change in end-of-life care processes, outcomes or spending.

A single-programme implementation report with no comparison group. It counts enrolment and service use and estimates no effect.

Implementation guidance drawn from six earlier comprehensive dementia care programmes. It reports no effect estimate of its own.

Direction is for the benefit redesign: projected out-of-pocket drug spending fell 55% ($56 to $25) for low-income-subsidy beneficiaries and 25% ($772 to $576) for others, with larger reductions for people with 6-8 comorbidities.

Admission showed no evidence of an effect on 30-day mortality or subsequent inpatient days, but raised 30-day health care spending by $2547. An instrumental-variable estimate for marginal admissions.

Direction is for co-existing Lewy body pathology in people with Alzheimer pathology: worse baseline cognition, faster global cognitive decline and more posterior hypometabolism than Alzheimer pathology alone. The seed amplification assay itself agreed closely with autopsy (96.3% sensitivity, 96.4% specificity in 61 cases).

A classification-validation study without a neuropathological reference standard, so accuracy cannot be judged. The groups behaved as expected: patients labelled LATE had mild amnestic impairment, limbic atrophy and stable MMSE over 30 months, while AD and AD/LATE groups declined.

Direction is for the test's accuracy against the reference standard; an accuracy result, not a health outcome. Driving features distinguished drivers with MCI from those with normal cognition (AUC 0.82), rising to 0.87 with demographics, APOE4 and cognition; drivers with MCI showed greater declines in trip frequency, night driving and route variety.

Advance care planning strongly increased DNR documentation (OR 14.12) but did not change whether residents died in the nursing home (OR 1.62, 95% CI 0.72-3.66). Evidence on other end-of-life outcomes was limited and inconsistent, and no study came from a non-Western setting.

The primary outcome did not improve. Emergency department visits and hospitalisations were lower (RR 0.45, 95% CI 0.31-0.65), which is a secondary outcome.

A Delphi consensus among 60 international expert panellists, reaching agreement on 15 major and 42 minor referral criteria. No patient outcome is measured and no effect is estimated.

Direction is for the test's accuracy against the reference standard; an accuracy result, not a health outcome. Cross-validated balanced accuracy of 70-95% and AUC above 78% across the six conditions; the model is a development-stage tool with one external memory-clinic validation sample.

A prognosis meta-analysis: it pools time to death and to nursing home admission and compares no exposure. Women's shorter survival was attributable to later age at diagnosis.

Three trials comparing respite with no respite found no significant benefit on any carer outcome; the four included trials were too different to pool.

The outcome is how prepared carers felt to decide about firearm access, not whether any injury was avoided.

Direction is for DREAMS START against treatment as usual: a 78% probability of being cost-effective at £20,000 per QALY, with cost and QALY differences individually non-significant. The clinical sleep result is in the table under its own row.

Direction is for amyloid: it induced hyperconnectivity from tau epicentres to posterior tau-vulnerable regions, present already in preclinical AD, and this hyperconnectivity mediated amyloid's effect on faster tau accumulation.

Direction is for greater spatial extent of tau: it tracked memory in unimpaired people and executive function in MCI and dementia better than a temporal meta-ROI, and tau spread fastest in unimpaired and MCI participants. Most amyloid-positive participants followed Braak staging, with substantial regional heterogeneity within each stage.

Direction is for regional tau burden: more tau went with less glucose metabolism (r = -0.49) and with worse domain-specific cognition, while amyloid was diffuse and only weakly related. An imaging association, not an exposure effect.

Direction is for going undiagnosed. Whether the diagnosis itself would change survival is not tested here.

Which intervention helped depended on severity: stimulation for cognition at any severity, training for global cognition in mild dementia, rehabilitation for function in mild dementia and for carer burden. Heterogeneity was high.

In dementia there may be small-to-moderate benefits at six months (low-certainty evidence, I2 88-96%); in MCI ginkgo probably has little or no effect (moderate certainty); in subjective cognitive complaints the effect is very uncertain. Adverse events were similar to placebo.

Pools 27 small trials in people who already have dementia, and reports a much larger effect (SMD 0.69) than the single largest such trial, DAPA, which found none.

The primary cognitive outcome was significantly WORSE in the exercise arm (adjusted difference -1.4, 95% CI -2.6 to -0.2, favouring usual care). The authors conclude the programme does not slow cognitive impairment and treat the difference as of uncertain clinical importance. Fitness did improve. This is the sharpest counterweight to the observational exercise evidence.

Direction is for antisense oligonucleotides lowering APP in neurons derived from people with an APP duplication or trisomy 21: reduced APP, rescued endolysosome and autophagy dysfunction and fewer intracellular and extracellular amyloid-β aggregates. Cell-culture work with no human outcome.

A retraction notice. It withdraws the 2006 Nature paper on Aβ*56 over figures showing "signs of excessive manipulation, including splicing, duplication and the use of an eraser tool", and reports no effect estimate.

An investigative news feature reporting signs of image fabrication in papers on the Aβ*56 amyloid oligomer. It is not a study of an outcome and reports no effect estimate.

A perspective review of arguments for and against the amyloid hypothesis, concluding that amyloid-beta is likely necessary but not sufficient and acts early as a trigger of tau-mediated neurodegeneration. It reports no effect estimate.

Phase 1 target-engagement result in 19 people; no clinical outcome measured.

The review's subject is the harm itself: brain swelling and microbleeds caused by the drugs.

Prespecified and post hoc re-analyses of a trial already reported elsewhere, so this is not independent evidence.

A statistically detectable but very small cognitive effect (ADAS-Cog SMD -0.11) alongside 107 more cases of ARIA-E per 1,000. The reviewers' own conclusion is that removing amyloid does not seem to produce clinically meaningful effects — the sharpest disagreement in this table with how the individual trials were reported.

Mechanistic multi-omic profiling of blood from three ARIA-positive patients and three matched controls on lecanemab. It describes a clonally expanded cytotoxic CD8+ T-cell signature and estimates no clinical effect.

Direction is for lecanemab in mice: it significantly reduced amyloid pathology and neuritic damage, an effect absent with Fc-silenced antibody or without microglia despite intact plaque binding. Mouse work with no human outcome.

An initial negative opinion was reversed on re-examination, with use restricted to APOE4 heterozygotes and non-carriers. The EPAR describes ARIA as affecting more than 1 in 10 people without giving a percentage.

Phase Ib/IIa biomarker result in 13 people; no cognitive outcome measured.

Against placebo: ARIA-E 24.4% vs 1.9%. Risk tracks APOE4 status and baseline imaging.

Direction is for the slower titration schedule against standard dosing, on the drug's own side effect. Amyloid reduction was comparable.

An open-label extension: after 18 months everyone is on the drug, so the comparison is early-start versus delayed-start, not drug versus placebo.

A single-clinic safety series with no comparison group. It reports how often ARIA and infusion reactions happened in practice, which is useful, but it cannot estimate an effect of the drug in either direction.

A mechanistic tissue study describing which microglial states accompany amyloid removal (TREM2 and APOE upregulation correlating with antibody response and clearance; complement signalling contributing). It estimates no effect of immunisation on a clinical outcome.

Corporate announcement discontinuing a product and terminating its confirmatory trial. It reports no clinical outcome, so no direction exists to record.

CHMP refused the drug, then on re-examination recommended it only for people with one or no APOE4 copy, where the ARIA rates are lower. Benefit on cognition and harm from ARIA in the same document, with the restriction as the regulator's way of balancing them.

Benefits were statistically present but every one fell below the minimum clinically important difference, against a number needed to harm of 9 for ARIA-oedema. Agrees with the Cochrane review and not with the trial reports.

Approved on amyloid reduction (surrogate) while reporting higher ARIA rates than placebo; the notice reports no cognitive outcome.

Less decline than placebo, alongside infusion reactions and ARIA.

Phase 1 dose-finding. The outcome is amyloid clearance; no cognitive outcome was measured.

Two identically designed trials disagreed: EMERGE met its primary endpoint, ENGAGE did not.

A coverage determination. It sets the conditions under which Medicare pays and reports no effect estimate.

Benefit is on the surrogate marker only: the approval rested on amyloid reduction, not on confirmed clinical benefit, and the confirmatory trial was later terminated.

Co-primary endpoints were not met at 52 weeks. The comparator was a low dose of the same drug rather than placebo, which the authors say masked any separation; they report separation in the MCI subgroup only at 78 and 104 weeks.

The primary endpoint was not met: the low dose showed no clinically meaningful benefit and the 3 mg dose showed 32% greater progression than placebo, with more serious adverse events. Less whole-brain volume loss on MRI is a surrogate finding.

The primary clinical endpoint (CDR-SB) was not met in the overall population. The tau figures are a biomarker outcome, not a clinical one.

ADAS-Cog11 showed slower decline, but the co-primary functional endpoint (ADCS-ADL) did not differ and the authors classify the study as negative.

Phase 1b safety and target-engagement result: adverse events were all mild or moderate with no serious events on MAPTRx, and CSF total tau fell dose-dependently by more than 50% in the two highest-dose groups. No clinical outcome was measured.

Direction is for STOPPING the antipsychotic: discontinuers were hospitalised less than matched continuers.

Direction is for discontinuation: tapering after 12 weeks lowered the 24-month absolute risk of delirium and fracture versus continuing, with no difference in stroke, pneumonia or death. Results were similar for abrupt discontinuation and after 24 weeks.

Wider range of harms than regulatory alerts had flagged, with the highest risks soon after starting. No increase in ventricular arrhythmia.

Direction is for valacyclovir: cognition worsened more on the drug than on placebo on the primary outcome (between-group difference 3.93 ADAS-Cog points, P = .01); function, amyloid PET and tau PET did not differ. The authors conclude it is not recommended.

No difference from placebo on the primary agitation outcome or other main behavioural outcomes. As-needed psychotropic use was lower during the active period, and no serious drug-related adverse events occurred.

Observational: 80% of residents were on no anti-dementia drug, so who gets prescribed and who does not may itself track prognosis.

Cholinesterase inhibitors, not memantine: -0.39 MMSE points a year against -2.50 with no treatment. The mortality benefit held only in the first year. Registry data with weighting, not a trial.

Primary outcome null. One secondary cognitive measure (ADAS-Exec) favoured liraglutide on an unadjusted test; ADCS-ADL and CDR-SB did not.

Direction is for AAVrh.10 delivery of APOE2 with the Christchurch mutation in mice: both vectors suppressed amyloid, but only the Christchurch variant also suppressed tau tangles and glial activation in tau mice and outperformed plain APOE2 behaviourally. Mouse work with no human outcome.

Direction is for peripheral cancer in AD mice: tumour-secreted cystatin-C bound amyloid oligomers and activated microglial TREM2, enabling degradation of existing plaques and rescuing cognition; the effect was abolished by microglial deletion or mutation of TREM2 or cystatin-C. Mouse work with no human outcome.

Direction is for lowering PU.1 in microglia, which reduced the severity of amyloid pathology in mice; microglia-specific CD28 deficiency did the opposite and increased plaque load. Mouse work with no human outcome.

A descriptive transcriptional atlas: it maps expression changes, isoform usage, co-expression modules and disease subtypes in microglia from post-mortem brains and estimates no effect of an exposure.

Direction is for deleting TIM-3 in microglia: it increased phagocytic activity, shifted microglia to the disease-associated state, reduced amyloid pathology and improved cognitive impairment in 5xFAD mice. Mouse work with no human outcome.

Direction is for blocking the ZBP1-RIPK1 axis: genetic deletion of Zbp1 or inhibition of RIPK1 attenuated neuroinflammation, amyloid pathology and behavioural deficits in AD mice, after showing that amyloid-induced oxidised mitochondrial DNA forms Z-DNA sensed by ZBP1 in microglia. Mouse work with no human outcome.

Direction is for removing the granzyme K-producing CD103-negative CD8+ T cells: their ablation ameliorated cognitive decline and reduced neuropathology in 3xTg-AD mice, and granzyme K caused neuronal dysfunction and tau hyperphosphorylation via PAR-1. Mouse and cell work with no human outcome.

Direction is for inhibiting C1q, C3 or the microglial receptor CR3, which reduced phagocytic microglia and early synapse loss; C1q was necessary for soluble amyloid-beta oligomers to damage synapses. Mouse work with no human outcome.

Direction is for NLRP3 or caspase-1 deficiency, which largely protected the mice from spatial memory loss and reduced amyloid deposition; the human data are limited to raised active caspase-1 in post-mortem MCI and Alzheimer brains.

The trial did not meet its primary endpoint at any of three doses despite sustained target engagement (lower CSF soluble TREM2, higher osteopontin); the most frequent adverse events were MRI changes resembling ARIA.

A regulatory enforcement action, not a study. The SEC's order finds the reported Phase 2 biomarker data were manipulated by an unblinded consultant and its complaint alleges the full patient data "showed no measurable cognitive improvement in the patients' episodic memory"; it estimates no effect.

Retraction notices for five PLOS ONE papers by Wang and colleagues, two co-authored with a Cassava Sciences employee. They withdraw the papers over blot-image integrity and estimate no effect.

The NPI-C agitation/aggression measure did not reach significance (p=0.094).

Not effective, and drug-related QT prolongation was observed. The randomised sample was smaller than planned.

A feasibility trial in 29 residents: designed to test whether the trial can be run, not powered for efficacy, and it reports no efficacy estimate.

The authors describe the reduction as small (-1.32 points).

A post hoc dementia subgroup of a randomised-withdrawal trial that was not designed or powered for it; 46 randomised responders. The authors say to read it cautiously.

Both doses beat placebo. Treatment-emergent adverse events were more common than placebo (84.6% at 2 mg, 76.8% at 1 mg, 73.8% placebo).

A mechanism study: it shows Arc packages tau into extracellular vesicles and that cell-to-cell tau transmission is almost absent in Arc knockout mice, with Arc levels correlating with phosphorylated tau in human AD brain vesicles. It tests no intervention and estimates no effect on an outcome.

Direction is for tau seeding activity: substantial hippocampal and neocortical seeding was present even without overt neocortical tangles and predicted region-specific cognitive performance and longitudinal decline; seeding and modification profiles tracked neuritic plaque density and separated AD from PART.

A model-building and screening study: it identifies over 500 genetic modifiers of tau propagation (including VPS29 and the UFMylation cascade) and shows UFMylation inhibition suppresses seeded propagation in vitro and in vivo. It estimates no effect on a clinical outcome.

Neither choir singing nor group music therapy beat standard care. Country was the strongest predictor of the differences between sites.

Improves depressive symptoms (moderate certainty) and overall behavioural problems (low certainty). No effect on agitation (SMD -0.05, 95% CI -0.27 to 0.17) and no evidence of long-term effects. Sits against the null MIDDEL trial on the same exposure.