Every row of the evidence table

The key point: the observational analysis showed light drinking looking protective, but the genetic (Mendelian randomisation) analysis did not, which the authors read as the protective appearance coming from people cutting down in early dementia.

This one reports light-to-moderate drinking as protective (HR 0.65) against non-drinking, and it flatly contradicts the Mendelian randomisation evidence. Infrequent drinkers were excluded, and non-drinkers include people who stopped for health reasons.

Sustained mild and moderate drinking carried lower risk than not drinking, sustained heavy drinking higher risk, and cutting down from heavy to moderate lower risk. Observational, with the same abstainer problem.

U-shaped: long-term abstainers had 47% higher risk than moderate drinkers, and above 14 units a week each extra 7 units raised risk by 17%. Neither end of the range looks like a benefit of drinking.

The exposure is cannabis use severe enough to need hospital care, not cannabis use in general, and the comparison is against other acute-care patients as well as the general population.

Direction is for QUITTING. Risk approached that of never-smokers and levelled off about seven years after quitting; weight gain after quitting narrowed the advantage. The authors flag residual confounding.

The two measures moved in opposite directions over 2015-2021: standardised incidence fell from 3.5% to 2.8% per year while prevalence rose from 10.5% to 11.8%; gaps between Black or Hispanic and White beneficiaries narrowed.

Direction is for more recent birth cohort: after controlling for age and period, later-born cohorts were less likely to have dementia in all three regions, more so among women; the point estimates for men in England were not significant.

Direction is for later birth cohort: each successive cohort had a significantly lower incident dementia rate, independent of sex, education and age.

Direction is for the later survey year: prevalence fell from 11.6% to 8.8%, with rising education associated with some of the decline despite a worse cardiovascular risk profile.

Direction is for later calendar epoch: incidence fell 44% from the first to the fourth epoch, but only among people with at least a high school diploma. The authors could not fully explain the decline.

Direction is for the later-born population: prevalence was 6.5% against the 8.3% expected from the earlier study (odds ratio 0.7), which the authors read as a cohort effect.

Incidence was consistently but non-significantly lower in the 2000 subcohort (rate ratio 0.75, 95% CI 0.56-1.02, borderline). The authors read the pattern, together with lower mortality and larger brain volumes, as suggesting a decline, but the primary comparison did not reach significance.

Direction is for degenerative pathology profiles: more than 80% had mixed pathologies, and of five clustered profiles the LATE-NC/hippocampal sclerosis and the ADNC/amyloid angiopathy profiles showed the fastest cognitive decline.

Direction is for LATE-NC: found in 64% of brains, stages 1a, 2 and 3 were associated with dementia and lower MMSE, it was among the strongest independent predictors of dementia, and its attributable risk (24.2%) exceeded that of Alzheimer's neuropathologic change (18.6%); it usually occurred alongside other pathologies.

Direction is for carrying the risk factors. The Danish estimate (37.8% across 16 factors) is lower than the Lancet Commission's global 45%.

Direction is for carrying the risk factors: depression, diabetes, low education, smoking, obesity, physical inactivity and alcohol overconsumption each independently raised the hazard of early-onset dementia, and most associations were stronger for early-onset than late-onset dementia.

Direction is for carrying the risk factors. Which factor mattered most differed by APOE risk group, on 2,065 cases split across 11 factors and three genetic strata, so the subgroup estimates are imprecise.

Direction is for carrying hypertension, diabetes or smoking. The attributable share rose with the age at which the factors were measured (22% at 45-54, 44% at 65-74), which is what you would expect if some of it is reverse causation rather than cause.

Direction is for carrying the risk factors: the Commission attributes 45% of cases to 14 modifiable factors, which is the same number read the other way as prevention potential. The Commission's own caveat is that "some associations might be only partly causal".

Direction is for carrying the risk factors. 39 candidate factors were screened against 485 cases, so individual estimates are imprecise.

Direction is for carrying the risk factors. The weighted combined estimate (32.0% for seven factors) is lower than the Lancet Commission's 45% for 14.

For the vascular risk factors: up to a quarter of the education-dementia association ran through hypertension, diabetes and related midlife factors, so carrying them accounted for part of the excess risk.

Direction is for carrying the peripheral diseases: together they were related to about one-third of global dementia burden, led by periodontal disease, chronic liver disease, hearing loss, vision loss and type 2 diabetes. Attributable fractions assume the pooled associations are causal.

A burden-of-disease decomposition: age-standardised rates rose slightly and population growth was the largest driver of the rise in cases. It compares no exposure, so no direction is recorded.

A lifetime-risk estimate (42% after age 55, higher in women, Black adults and APOE4 carriers) and a projection of new cases. It compares no exposure, so no direction is recorded.

A pooled incidence and prevalence estimate with no exposure compared, so no direction is recorded.

A prevalence estimate and forecast: cases are projected to rise from 57.4 million to 152.8 million while age-standardised prevalence stays flat, with the rise attributed to population growth and ageing. It compares no exposure, so there is no direction to record.

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

Direction is for being African-American or American Indian/Alaska Native relative to Asian-American members: incidence was highest in those groups (26.6 and 22.2 per 1000 person-years) and lowest in Asian-Americans (15.2). The authors present this as a benchmark for reducing disparities, not as a biological effect of race.

A position paper from an expert network. It sets out 12 priority research areas on sex and gender in Alzheimer's disease and reports no effect estimate.

Direction is for female sex: at higher amyloid levels women had higher plasma p-tau217 than men, greater tau deposition and accumulation at a given p-tau217 level, and faster cognitive decline in two of the cohorts.

Direction is for female sex: women had higher odds of a high neuritic plaque burden than men after adjustment, and were more likely to reach Braak stage V-VI. Black non-carriers and non-carriers of African ancestry were least likely to have high plaque burden, a protection weakened in ε4 carriers.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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