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 Swedish study of over 1,200 people with memory symptoms found that a blood test combining p-tau217 with an amyloid ratio (the 'Amyloid Probability Score 2') was far more accurate at identifying Alzheimer's disease than doctors' clinical judgment alone.
Why it matters
A blood test combining p-tau217 and an amyloid ratio identified Alzheimer's disease with 91% accuracy in symptomatic patients, compared with 73% for dementia specialists and 61% for primary care doctors. The study demonstrates improved diagnostic accuracy but does not establish whether this more reliable detection leads to better treatment outcomes.
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68/100
Baseline plasma VEGFA and PGF each showed a significant interaction with amyloid burden on prospective cognitive decline.
Why it matters
In people with elevated amyloid, low plasma VEGFA and high plasma PGF were linked to greater cognitive decline and faster accumulation of tau over time. This suggests these blood markers may help flag who is at risk of progressing in preclinical Alzheimer's disease, but it does not show that changing them treats, cures or prevents the disease.
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This observational study analyzed electronic health records of about 1.09 million US patients with type 2 diabetes and found that those prescribed semaglutide (a GLP-1 diabetes/weight-loss drug) were substantially less likely to receive a first-time Alzheimer's diagnosis over 3 years than those on other diabetes medications.
Why it matters
In this observational analysis of health records, people with type 2 diabetes prescribed semaglutide were less likely to receive a first-time Alzheimer's diagnosis over 3 years than those on other diabetes drugs. The authors state this cannot establish cause and effect, and a later randomized trial did not confirm a clinical benefit in people who already had early Alzheimer's disease.
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In this randomized clinical trial, BIIB080 reduced tau biomarkers, including CSF t-tau, CSF p-tau181, and tau PET, which is associated with cognitive decline, in participants with mild AD.
Why it matters
In this trial of 46 participants with mild Alzheimer disease, BIIB080 was generally well tolerated and produced dose-dependent reductions in cerebrospinal fluid t-tau and p-tau181, with reduced tau PET accumulation versus placebo at week 25. These are biomarker results in a small early trial and do not yet show that the treatment improves symptoms or changes the course of the disease.
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Blood-based biomarkers hold great promise to revolutionize the diagnostic and prognostic work-up of Alzheimer's disease (AD) in clinical practice.
Why it matters
This review states that several assays measuring phosphorylated tau in plasma show high diagnostic accuracy in distinguishing Alzheimer's disease from other neurodegenerative diseases in patients with cognitive impairment, and that prognostic models based on plasma p-tau can predict future development of Alzheimer's dementia in people with mild cognitive complaints. It says using such assays in specialist memory clinics would reduce the need for more costly CSF or PET investigations, and that longitudinal measurements will help detect disease-modifying effects of new drugs or lifestyle interventions.
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Alzheimer's disease (AD), the leading cause of dementia, has an estimated heritability of approximately 70% 1 .
Why it matters
By comparing exome sequencing data from over 32,000 people, this study found that rare damaging variants in ATP8B4 and ABCA1 were significantly associated with Alzheimer's disease risk, in addition to variants in TREM2, SORL1 and ABCA7. The results add evidence for roles of amyloid-beta precursor protein processing, amyloid-beta aggregation, lipid metabolism and microglial function in Alzheimer's disease.
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The risk of mild cognitive impairment (MCI) or dementia in individuals with subjective cognitive decline (SCD) and biomarkers indicating Alzheimer disease (AD) pathology in comparison with individuals with SCD without biomarker evidence for AD is critical to delineate the potential role of biomarker assessment in this group.
Why it matters
This meta-analysis examined whether people with subjective cognitive decline who have Alzheimer's disease biomarkers are more likely to progress to mild cognitive impairment or dementia. It is a review of observational studies and does not test any treatment, cure, or prevention.
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Baseline plasma GFAP could detect abnormal CSF Aβ42/40 and CSF Aβ42/T-tau with an AUC of 0.79 (95% CI 0.72-0.86) and 0.80 (95% CI 0.72-0.86), respectively.
Why it matters
In 160 people who already had mild cognitive impairment and were followed for an average of 4.7 years, a baseline blood GFAP level picked out abnormal spinal-fluid Alzheimer markers with moderate accuracy (AUC 0.79–0.80) and predicted who later developed Alzheimer dementia (AUC 0.84). This is a single-cohort study of a blood marker for detection and prediction in people with MCI, not a diagnosis on its own, a treatment, or a test validated in people without memory problems.
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The clinical diagnosis of probable AD dementia demonstrated good agreement with biologically defined AD (positive predictive value 85.2%).
Why it matters
In this cohort, clinical diagnosis of probable Alzheimer dementia agreed well with biologically defined Alzheimer disease, and biologically defined disease was more frequent with older age and APOE ε4. This is about how often biomarker-defined disease occurs and does not test any treatment, cure, or prevention.
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In this study, elevated [18F]RO948 SUVRs were most often seen among Aβ-positive cases, which suggests that [18F]RO948 has high specificity for AD-type tau and highlights its potential as a diagnostic marker in the differential diagnosis of AD.
Why it matters
Among 613 people, [18F]RO948 tau PET separated Alzheimer dementia from cognitively unimpaired people (AUC 0.98) and from non-Alzheimer disorders (AUC 0.97). That beat the best MRI measures (0.91 and 0.80) and was a little ahead of the best CSF measures (0.94 and 0.93). The authors say high readings were "most often seen among Aβ-positive cases", which "suggests that [18F]RO948 has high specificity for AD-type tau". They describe its "potential" for diagnosis. These figures are for people who already had dementia, not for the early (MCI) stage, and this is a diagnostic study, not a treatment.
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SUVr abnormality was most frequently observed in cingulate, followed by orbitofrontal, precuneal, and insular cortices and then the associative, temporal, and occipital regions.
Why it matters
This study developed a model for staging cortical amyloid deposition using PET, finding that amyloid abnormality appeared first in the cingulate and then spread to other regions. It is about staging and measurement, not about treating, curing, or preventing Alzheimer disease.
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The large number of participants screened with amyloid positron emission tomography (PET) and standardized assessments provides an unprecedented opportunity to evaluate factors associated with elevated brain amyloid.
Why it matters
Of 4,486 clinically normal older adults (average age 71) who had an amyloid PET scan while screening for an Alzheimer's prevention trial, 1,323 (29.5%) had elevated brain amyloid, which was linked with a family history and the APOE ε4 gene but "not with multiple other previously reported risk factors". People with elevated amyloid scored lower on a cognitive test composite and reported more "subtle recent declines in daily cognitive function", which the authors say supports elevated amyloid being "an early stage in the Alzheimer continuum" and shows such people can be enrolled in prevention trials. These are one-time screening measurements from trial volunteers, so the study does not show who will go on to develop dementia, and it reports no treatment.
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This study shows that PUTG component scores were significantly associated with diagnostic group and AD biomarkers, a finding that was more pronounced in APOE ε4 carriers.
Why it matters
In blood samples from 689 older adults in the Alzheimer's Disease Neuroimaging Initiative, two groupings of triglycerides built from long-chain polyunsaturated fatty acids were lower in people with mild cognitive impairment or Alzheimer's disease than in cognitively normal people. These were also linked to hippocampal volume and entorhinal cortical thickness on MRI, and, in APOE ε4 carriers, to spinal-fluid β-amyloid 1-42. This is an observational, one-time-point comparison of specific lipid species: it does not show that blood fats cause Alzheimer's or that changing diet or triglyceride levels would affect it.
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Moreover, biomarker plasma levels and rates of change over time of participants who developed Alzheimer's disease dementia during follow-up were compared with age and sex-matched dementia-free control subjects.
Why it matters
This population-based cohort study found that higher baseline plasma amyloid-β42 was associated with lower risk of developing all-cause or Alzheimer's disease dementia, while higher baseline plasma neurofilament light chain was associated with higher risk. Combining the lowest amyloid-β42 quartile with the highest neurofilament light chain quartile was associated with a much stronger risk of dementia, and neurofilament light chain levels increased faster in those who developed Alzheimer's disease.
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As one of few meta-analyses comparing different quantities of physical activity and exercise interventions for AD in details, our study suggests that physical activity and exercise can improve cognition of older adults with AD.
Why it matters
This meta-analysis of 13 randomised controlled trials found that physical activity and exercise improved cognition in people with Alzheimer's disease, as measured by MMSE scores. Subgroup analyses suggested that different amounts of activity produce different effects.
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These results suggest that increasing levels of tau most consistently relate to declines in cognition preceding biomarker collection.
Why it matters
In 152 people who were cognitively normal or very mildly impaired, brain scans for tau, amyloid and hippocampal size were each linked to earlier cognitive decline. When the three were analysed together, only tau stayed a significant predictor, and decline was steepest in people with high levels of all three. The authors say this suggests amyloid alone "may be insufficient to produce cognitive change" and supports using several biomarkers together to stage Alzheimer's, but the decline was measured before the scans were taken, so these are associations, not predictions or treatments.
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Although brain neuroinflammation may play an instrumental role in the pathophysiology of Alzheimer's disease, its actual impact on disease progression remains controversial, being reported as either detrimental or protective.
Why it matters
This longitudinal study used PET imaging to examine the relationship over time between microglial activation and clinical progression in people with Alzheimer's disease. It is an observational imaging study and does not test any treatment, so it says nothing about curing or preventing Alzheimer's disease.
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Elecsys CSF biomarker assays may provide reliable alternatives to PET in Alzheimer's disease diagnosis.
Why it matters
Cutoffs for a fully automated spinal-fluid test were set against amyloid PET scans in a Swedish cohort (277 people), then applied unchanged in the separate ADNI cohort (646 people), where the test agreed with the scan's yes/no answer 89%–90% of the time. People with mild cognitive impairment who tested positive showed greater clinical decline over 2 years. The authors conclude such tests "may provide reliable alternatives to PET" for diagnosis; the study tested no treatment.
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68/100
Baseline biomarkers largely do not predict risk for developing ARIA-E. ARIA-E was associated with significant longitudinal changes in several biomarkers, with larger reductions in amyloid PET and CSF p-tau and t-tau concentrations, and paradoxically greater hippocampal volume reduction and ventricular enlargement, suggesting that ARIA-E in bapineuzumab-treated cases may be related to increased Aβ efflux from the brain and affecting downstream pathogenic processes.
Why it matters
In phase 3 bapineuzumab trials (1,512 people with mild to moderate Alzheimer's who had biomarker tests; 154 developed brain swelling called ARIA-E), baseline amyloid PET, CSF and MRI measures largely did not predict who would develop ARIA-E. By week 71, treated participants with ARIA-E showed larger drops in amyloid PET and CSF p-tau and t-tau, but also "paradoxically greater hippocampal volume reduction and ventricular enlargement". The authors suggest ARIA-E may reflect increased amyloid clearance from the brain. This is a biomarker comparison, not a randomized one, and it does not show that bapineuzumab or ARIA-E benefits patients.
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Twelve articles-published between the 2007 and 2017-have been included in this systematic review after a quantitative and qualitative selection.
Why it matters
A review of twelve studies found that a machine-learning method called random forest, applied to combined imaging data, produced some of the best accuracy for predicting conversion from mild cognitive impairment to Alzheimer's disease. This is about improving prediction, not about treating or curing the disease.
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Men have a shorter life expectancy compared with women but the underlying factor(s) are not clear.
Why it matters
This case-control study tested whether lifetime-acquired loss of chromosome Y in blood cells is associated with Alzheimer's disease. It reports an association only and does not show any treatment, cure or prevention.
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Voxel-wise contrasts against controls (at P < 0.05 family-wise error corrected) showed that (18)F-AV1451 and (18)F-FDG patterns in patients with posterior cortical atrophy ('visual variant of Alzheimer's disease', n = 7) specifically targeted the clinically affected posterior brain regions, while (11)C-PiB bound diffusely throughout the neocortex.
Why it matters
This preliminary study found that tau PET imaging patterns were regionally associated with clinical and anatomical differences in Alzheimer's disease, unlike amyloid-beta imaging. It does not test a treatment or cure, but suggests tau imaging may help relate brain changes to symptoms.
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Brain iron elevation is implicated in Alzheimer's disease (AD) pathogenesis, but the impact of iron on disease outcomes has not been previously explored in a longitudinal study.
Why it matters
In the ADNI cohort, higher baseline cerebrospinal fluid ferritin levels were linked to worse cognitive performance over 7 years and predicted conversion from mild cognitive impairment to Alzheimer's disease, and ferritin was elevated by the APOE-ɛ4 risk allele. This points to brain iron elevation as a possible mechanism, but it does not show that lowering iron treats or prevents the disease.
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Brain DNA methylation in multiple AD loci is associated with AD pathologies.
Why it matters
In 740 autopsied participants, DNA methylation in SORL1, ABCA7, HLA-DRB5, SLC24A4, and BIN1 was associated with a pathological diagnosis of Alzheimer disease, and the association held for amyloid load and tau tangle density. This links epigenetic changes in known risk genes to disease pathology but does not test any treatment, cure, or prevention.
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Plasma amyloid-β (Aβ) peptide levels have been examined as a low-cost accessible marker for risk of incident Alzheimer's disease (AD) and dementia, but results have varied between studies.
Why it matters
This study found that higher plasma amyloid-β1-42 levels were associated with lower risk of dementia in older adults followed for about 7.6 years. It is observational and does not show that measuring or altering plasma amyloid-β prevents 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.
- Relevance of magnetic resonance imaging for early detection and diagnosis of Alzheimer disease
- Proteomics of brain, CSF, and plasma identifies molecular signatures for distinguishing sporadic and genetic Alzheimer's disease
- Diagnostic accuracy of cerebrospinal fluid biomarkers measured by chemiluminescent enzyme immunoassay for Alzheimer disease diagnosis
- Prediction and classification of Alzheimer disease based on quantification of MRI deformation
- Preclinical Alzheimer's disease biomarkers accurately predict cognitive and neuropathological outcomes
- Alzheimer-type neuropathology and clinical symptoms of dementia in mentally retarded people without Down syndrome
- Evaluation of preanalytical factors on quantification of amyloid-β (1-42), phosphorylated tau 181, and total tau in cerebrospinal fluid
- Widespread brain tau and its association with ageing, Braak stage and Alzheimer's dementia
- Epidemiology, Pathophysiology, and Imaging of Atherosclerotic Intracranial Disease
- A phase Ib multiple ascending dose study of the safety, tolerability, and central nervous system availability of AZD0530 (saracatinib) in Alzheimer's disease