Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.
Highest usefulness score first. Studies without a score come last.
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This study found no effect of ongoing BDZR use on ADAS-Cog scores in those with mild to moderate AD over 18 months.
Why it matters
In this study, ongoing use of benzodiazepines and related drugs was not associated with greater cognitive decline over 18 months in people with mild to moderate Alzheimer disease. It addresses whether these medications worsen decline, not whether they treat, cure or prevent the disease.
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64/100
The prevalence of A+T+N+F+ profile was 66.24% in clinically diagnosed AD dementia patients; similarly, the majority of individuals with reduced FDG-PET were AD dementia subjects.
Why it matters
This longitudinal study examined FDG-PET as a possible independent biomarker in 551 individuals with Alzheimer's disease biomarker profiles. It found that individuals with reduced FDG-PET performed worse and declined faster on cognitive tests and had faster shrinking of the middle temporal lobe, suggesting FDG-PET may add information beyond the ATN framework.
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Alzheimer's disease (AD), the most common cause of dementia, has long been associated with bacterial infections and inflammation-causing immunosenescence.
Why it matters
The gut bacteria of people with Alzheimer's disease differed from those without dementia, with fewer butyrate-producing bacteria and more types linked to inflammation. This is an observed association and does not show that changing the microbiome treats or prevents Alzheimer's disease.
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This study analyzed 80,660 single-nucleus transcriptomes from the prefrontal cortex of 48 individuals with varying degrees of Alzheimer's disease pathology to examine molecular and cellular changes across six major brain cell types.
Why it matters
Reports a single-cell transcriptomic analysis of Alzheimer's disease.
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64/100
Our main findings were: (i) FDG-PET uptake in the bilateral anterior cingulate cortex and anterior temporal pole was associated with baseline global cognition in cognitively stable 80+ (the resilience signature); (ii) established Alzheimer's disease imaging biomarkers did not predict baseline global cognition in this subset of participants; (iii) in the full MCSA 80+ and ADNI cohorts, amyloid burden and FDG-PET in the resilience signature were the stronger predictors of baseline global cognition; (iv) sex and systemic vascular health predicted FDG-PET in the resilience signature, suggesting vascular health maintenance as a potential pathway to preserve the metabolism of these areas; and (v) the resilience signature provided significant information about global longitudinal cognitive change even when considering amyloid status in both the MCSA and ADNI cohorts.
Why it matters
In cognitively stable people aged 80 and over, FDG-PET uptake in the anterior cingulate cortex and anterior temporal pole was linked to baseline cognition and to later cognitive change, while established Alzheimer's imaging biomarkers did not predict baseline cognition in this group. The findings suggest vascular health maintenance as a possible pathway to preserve metabolism in these areas, but this is not yet shown to prevent or treat Alzheimer's disease.
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Massive parallel sequencing recently allowed the identification of three genes carrying a higher burden of rare, protein-truncating and missense predicted damaging variants in Alzheimer disease (AD) cases as compared to controls: TREM2, SORL1, and ABCA7.
Why it matters
This meta-analysis of sequencing data found that rare SORL1 coding variants are associated with Alzheimer's disease risk at the gene level. It identifies a genetic risk factor but does not provide a treatment, cure or prevention.
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Our findings indicate that tau accumulates even in amyloid-negative healthy OA and this process can be measured with in vivo tau-PET.
Why it matters
This longitudinal PET study found that tau accumulates over time even in healthy older adults who do not have amyloid, and that tau increases faster in people with Alzheimer disease. It suggests tau buildup can be tracked in living people, but it does not test any treatment or show that lowering tau changes outcomes.
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Plasma Abeta42/Abeta40 ratio has potential as a prescreener to identify Alzheimer pathological changes in cognitively normal individuals with SCD.
Why it matters
In people with subjective cognitive decline, a low ratio of two amyloid proteins in the blood was linked to abnormal amyloid in the brain and to a higher risk of progressing to mild cognitive impairment or dementia. This blood test might help screen for early Alzheimer's changes, but it is not a treatment or cure.
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The diagnostic performance of plasma biomarkers was poor (area under the curve [AUC] between 0·53 [95% CI 0·44-0·62] and 0·74 [0·66-0·82]) except for plasma NfL concentrations, which had an AUC of 0·88 (0·82-0·93) for the differentiation of the asymptomatic group versus the prodromal Alzheimer's disease group and 0·95 (0·92-0·98) for the asymptomatic group versus the Alzheimer's disease dementia group.
Why it matters
In adults with Down syndrome, plasma neurofilament light performed well at distinguishing asymptomatic people from those with prodromal or dementia-stage Alzheimer's disease, while most other plasma biomarkers performed poorly. This supports plasma NfL for early detection, not for treating, curing, or preventing Alzheimer's disease.
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We envision that defining AD as a biological construct will enable a more accurate characterization and understanding of the sequence of events that lead to cognitive impairment that is associated with AD, as well as the multifactorial etiology of dementia.
Why it matters
This 2018 NIA-AA paper proposes, for research use, defining Alzheimer's disease by biology rather than by symptoms alone. Its authors "envision" that this will give a more accurate picture of "the sequence of events that lead to cognitive impairment" and of the "multifactorial etiology of dementia", but this is a stated aim, not a tested result. The paper reports no patient data and offers no test, treatment or cure.
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Genetic risk factors of AD dementia demonstrate effects related to Aβ, as well as synergistic interactions with Aβ.
Why it matters
In 702 participants, APOE ε4 was strongly related to baseline amyloid and to memory decline and hippocampal shrinkage in those with amyloid, while a broader polygenic risk score showed only weak links to amyloid. This describes genetic influences on disease markers and does not test any treatment.
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Memory decline accompanies Aβ accumulation in otherwise healthy, Aβ-negative older adults.
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Vascular health had quantifiably greater impact on neurodegeneration in AD regions than on amyloid deposition.
Why it matters
In 430 adults over 60 from the Mayo Clinic Study of Aging, people with at least one cardiovascular or metabolic condition (such as high blood pressure, high cholesterol, diabetes or stroke) showed more brain-tissue loss on scans. Their levels of amyloid or entorhinal tau were no different from people without those conditions. In the study's models, vascular health was linked to neurodegeneration but not to amyloid, and high cholesterol specifically was linked to entorhinal tau. This is an observational imaging study that counted diagnoses from health records; it did not test whether treating these conditions changes Alzheimer's.
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The heterogeneity of Alzheimer's disease contributes to the high failure rate of prior clinical trials.
Why it matters
This analysis used a clustering algorithm on 5-year data from 562 people with mild cognitive impairment to identify groups with different cognitive trajectories. It describes prognostic clusters, not a treatment, cure or prevention.
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Protection from these ADP factors may be important for aging without significant ADP.
Why it matters
In this population-based sample, midlife dyslipidemia was the only factor besides demographics and APOE genotype associated with amyloid deposition, while obesity, smoking, diabetes, hypertension, and cardiac and metabolic conditions were linked to greater Alzheimer's-pattern neurodegeneration. Among those 85 and older, several variables showed small to moderate effects in predicting aging without significant Alzheimer's pathology.
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Secondary analysis suggested that this effect may be driven primarily by individuals who are negative for the established AD genetic risk factor, apolipoprotein E (APOE) ɛ4.
Why it matters
Certain HLA gene variants were associated with higher spinal fluid amyloid levels and, in a subset, with a marker of inflammation, possibly mainly in people without the APOE ε4 risk factor. This is a case-control genetic study and does not test treatment or prevention.
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Amyloid protein precursor (APP), presenilin-1 (PSEN1), and presenilin-2 (PSEN2) mutations cause autosomal dominant forms of early-onset Alzheimer disease (AD-EOAD).
Why it matters
This genetic screening study updated the number of families with APP, PSEN1, or PSEN2 mutations causing early-onset Alzheimer's disease. It adds to knowledge about inherited forms and the challenge of classifying variants, but it does not test a treatment or cure.
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Among the 174 participants (81 men [46.6%]; 93 women [53.4%]; mean [SD] age, 65.7 [8.9] years), a proportion (14%-17%) of individuals with neurodegeneration alone (SNAP) later demonstrated Aβ+.
Why it matters
Among 174 participants, a proportion (14%-17%) of individuals with neurodegeneration alone later showed amyloid positivity. This describes how biomarker status can change over time in preclinical Alzheimer's disease and does not test any treatment, cure or prevention.
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CSF Aβ42 levels are tightly coupled with cortical amyloid load in the earliest stages of preclinical AD, and begin to decrease dramatically prior to the point when an abnormal threshold of cortical accumulation is detected with amyloid imaging.
Why it matters
Among 164 cognitively normal people, those whose amyloid PET scan changed from negative to positive over follow-up had lower cerebrospinal fluid Aβ42 at baseline than those who stayed negative but higher than those already positive. This describes very early biomarker changes in preclinical Alzheimer's disease and does not test any treatment or prevention.
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Biomarkers have become an essential component of Alzheimer disease (AD) research and because of the pervasiveness of AD pathology in the elderly, the same biomarkers are used in cognitive aging research.
Why it matters
This 2016 paper proposes the "A/T/N" scheme, which sorts seven Alzheimer's biomarkers into three groups: A for amyloid (amyloid PET or CSF Aβ42), T for tau (CSF phospho-tau or tau PET) and N for neurodegeneration (FDG-PET, structural MRI or CSF total tau). Each group is rated positive or negative, giving profiles such as A+/T+/N−. The authors present it as a descriptive research shorthand that makes no assumption about which changes come first and is "not a diagnostic classification system"; it reports no patient data and is not about treatment.
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Implementation of amyloid biomarkers in clinical practice would be accelerated if such biomarkers could be measured in blood.
Why it matters
In 719 people from the Swedish BioFINDER cohort, ranging from cognitively healthy to Alzheimer's dementia, blood levels of amyloid (Aβ42 and Aβ40) agreed only weakly with spinal-fluid levels and were clearly lower only at the dementia stage; in earlier stages Aβ42 was "just moderately decreased" and Aβ40 "unchanged". Higher blood (but not spinal-fluid) amyloid was associated with white matter lesions, microbleeds, hypertension, diabetes and heart disease. This is an early look at blood amyloid as a possible test: it reports associations in one research cohort, gives no diagnostic accuracy figures, and tested no treatment.
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64/100
Although the prevalence of dementia continues to increase worldwide, incidence in the western world might have decreased as a result of better vascular care and improved brain health.
Why it matters
This review notes that although dementia prevalence continues to increase worldwide, incidence in the western world might have decreased as a result of better vascular care and improved brain health, and that researchers are moving away from the simple linear causality of the original amyloid hypothesis. It reports moderately positive results for interventions targeting several lifestyle factors in non-demented elderly patients and moderately positive interim results for lowering amyloid in pre-dementia Alzheimer's disease.
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Considering several covariates together allowed the identification of responders.
Why it matters
In this 9-week trial of 186 patients with Alzheimer's disease and agitation, response to citalopram varied across patient subgroups, with some more likely to benefit and others more likely to do better on placebo. This means treatment effects are not uniform, and it does not identify a way to cure or prevent Alzheimer's disease.
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Previous studies have evaluated gene expression in Alzheimer's disease (AD) brains to identify mechanistic processes, but have been limited by the size of the datasets studied.
Why it matters
By analyzing gene expression across many brain samples, this meta-analysis identified thousands of differentially expressed genes and highlighted pathways such as nitric oxide and reactive oxygen species in macrophages, NFkB, and mitochondrial dysfunction. It identifies possible disease processes but does not test or show any treatment, cure, or prevention.
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Substantial variability occurs in the prevalence of "PiB-positive" studies in subjects with Parkinsonism and cognitive impairment.
Why it matters
This systematic review of amyloid PET studies found that about 41% of people across Parkinson's disease with dementia, Parkinson's disease with mild cognitive impairment, and dementia with Lewy bodies were amyloid-positive. It describes how often amyloid is present in these related conditions and does not test treating, curing, or preventing Alzheimer's disease.
From across this topic
10 of the 5,172 studies in this topic, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
- Conversion of amyloid positive and negative MCI to AD over 3 years: an 11C-PIB PET study
- A soluble phosphorylated tau signature links tau, amyloid and the evolution of stages of dominantly inherited Alzheimer’s disease
- The bivariate distribution of amyloid-β and tau: relationship with established neurocognitive clinical syndromes
- Plasma Aβ42 and Total Tau Predict Cognitive Decline in Amnestic Mild Cognitive Impairment
- A neurocognitive speech taxonomy for voice biomarkers of Alzheimer's disease
- Identification and validation of novel cerebrospinal fluid biomarkers for staging early Alzheimer's disease
- A cerebrospinal fluid synaptic protein biomarker for prediction of cognitive resilience versus decline in Alzheimer's disease
- Clinical Benefits and Risks of Antiamyloid Antibodies in Sporadic Alzheimer Disease: Systematic Review and Network Meta-Analysis With a Web Application
- Structural Brain Correlates With Appetite and Eating Disturbances Across the Alzheimer Disease Spectrum
- The Alzheimer disease protective mutation A2T modulates kinetic and thermodynamic properties of amyloid-β (Aβ) aggregation