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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We performed a systematic review and meta-analysis to explore whether type 2 diabetes mellitus (T2DM) increases the risk of Alzheimer's disease (AD).
Why it matters
This systematic review and meta-analysis found that type 2 diabetes was associated with an increased risk of Alzheimer's disease, with a pooled adjusted risk ratio of 1.57, and that the increased risk seemed to be mediated through cerebrovascular pathology such as cerebral infarcts. It identifies diabetes as a risk factor but does not show that treating diabetes prevents or cures Alzheimer's disease.
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Association of HT use and risk of AD may depend on timing of use.
Why it matters
In 1,768 women followed in the Cache County Study, those who started any hormone therapy within 5 years of menopause had 30% less risk of Alzheimer's disease (95% CI 0.49–0.99), while those who started 5 or more years later saw no reduction. Women who began combined estrogen-progestin therapy in later life had higher rates (hazard ratio 1.93, though the 95% CI of 0.94–3.96 includes no effect), similar to the 2.05 ratio reported in randomized trials. Because this is an observational study, it suggests timing may matter. It does not show that hormone therapy prevents Alzheimer's.
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Cerebrospinal fluid biomarkers may be useful to monitor the effects of novel disease-modifying anti-Aβ drugs in clinical trials.
Why it matters
In these phase 2 trials, bapineuzumab was associated with a decrease in cerebrospinal fluid T-tau and P-tau compared to baseline, with the difference reaching statistical significance for P-tau. This shows an effect on biomarkers of neuronal degeneration and tau-related pathology, not on clinical outcomes.
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We identified a new genetic risk association of AD with rare coding CLU variations that is independent of the 5' common association signal identified in the GWA studies.
Why it matters
This genetic study found that both common and rare variations in the CLU gene were associated with increased risk of Alzheimer disease across several cohorts. These are risk associations only and do not provide a treatment or cure.
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Subjects were 404 persons in the Religious Orders Study, a cohort study of aging, who underwent annual clinical evaluations, including 19 neuropsychological tests from which 5 cognitive domain and global summary scores were derived, and brain autopsy at time-of-death (mean age-at-death 86).
Why it matters
This cohort study of 404 older persons examined how the severity of cerebral amyloid angiopathy relates to cognitive domains. It describes an association between a vascular pathology and cognition and does not test a treatment, cure, or prevention.
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The Alzheimer's Disease Neuroimaging Initiative has successfully recruited cohorts of cognitively normal subjects, subjects with mild cognitive impairment (MCI), and subjects with Alzheimer disease with anticipated baseline characteristics.
Why it matters
This paper describes the 819 people (229 cognitively normal, 398 with mild cognitive impairment, 192 with mild Alzheimer's) who were followed for 12 months in the Alzheimer's Disease Neuroimaging Initiative, so that later studies could test brain-scan and fluid biomarkers against them. In this group, people with MCI progressed to dementia "at a rate of 16.5% per year", and baseline spinal-fluid Abeta-42 "separated the 3 groups as expected and successfully predicted the 12-month change in cognitive measures". It is an observational description of one research cohort over one year. It tests no treatment, and about half the MCI group were already on antidementia drugs.
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The efficacy, safety and disease-modification of tramiprosate (homotaurine)were investigated in a recently completed large-scale Phase III clinical study in patients with mild to moderate Alzheimer's disease (AD), the Alphase study.
Why it matters
This was a subgroup analysis of a large double-blind, randomized, placebo-controlled trial testing tramiprosate in mild-to-moderate Alzheimer's disease, using hippocampal MRI measurements to assess disease modification. The provided text does not report the results, so it is unknown whether tramiprosate affected brain volume, cognition, or clinical outcomes.
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The amyloid-beta peptide Abeta(42) has been implicated in the pathogenesis of Alzheimer's disease (AD).
Why it matters
In this 12-month phase II trial, 210 patients with mild to moderate Alzheimer's disease took tarenflurbil, a drug intended to lower amyloid-beta 42, or placebo. The study was designed to test effects on cognition and function; it is an early-phase trial and does not establish that the drug works.
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68/100
The APOE*E4 allele of the gene for apolipoprotein E (APOE) has been reported as a risk factor for Alzheimer disease (AD) to varying degrees in different ethnic groups.
Why it matters
This cross-national study found that the APOE*E4 allele was associated with Alzheimer disease at similar strength in Indian and US samples, though Alzheimer's prevalence was very low in the Indian site. It describes a risk association and offers no treatment, cure or prevention.
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This study demonstrated statistically significant differences between physostigmine and placebo on both a performance-based cognitive functioning instrument and a clinician's global evaluation.
Why it matters
In this trial, controlled-release physostigmine produced small improvements on two primary symptom measures in some patients with mild to moderate Alzheimer's disease, but no significant improvement on secondary measures. The drug was also linked to more patients dropping out and more side effects like nausea and vomiting.
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These data suggest the following: (1) patients with mild cognitive impairment can be clinically defined, (2) many members of this group progress to Alzheimer's disease, and (3) APOE epsilon 4 allele status appears to be a strong predictor of clinical progression.
Why it matters
In 66 people with mild cognitive impairment from the Mayo Clinic Alzheimer's Disease Patient Registry, followed for up to 54 months, 24% had developed dementia at about 18 months, 44% at 36 months (36 people re-seen) and 55% at 54 months (22 people re-seen). In a multivariate analysis, carrying an APOE ε4 allele was "the strongest predictor of clinical outcome", but the summary gives no measure of how much it raised risk. This is an observational study of who progressed; it did not test any treatment and does not show that APOE status decides any one person's outcome.
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The Consortium to Establish a Registry for Alzheimer's Disease (CERAD) has developed brief, comprehensive, and reliable batteries of clinical and neuropsychological tests for assessment of patients with the clinical diagnosis of Alzheimer's disease (AD).
Why it matters
CERAD built short, standardised sets of clinical and memory/thinking tests for Alzheimer's disease and gave them to more than 350 people with a clinical diagnosis of AD and 275 controls at 16 university centres. The tests told apart people without dementia from those with mild and moderate dementia, picked up decline in language, memory, praxis and general intellectual status after one year, and gave consistent results between raters and on retesting. The authors cautioned that validation was still limited and that diagnoses were awaiting confirmation at postmortem examination, so this paper shows that the tests were usable and consistent, not that they diagnose AD.
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In a pooled sample of multiple selected cohorts of cognitively unimpaired older adults, higher plasma p-tau217 levels were consistently associated with increased risk of clinical progression and accelerated cognitive decline.
Why it matters
In this pooled analysis of older adults without cognitive impairment, higher baseline blood p-tau217 levels were linked to a higher risk of progressing to cognitive impairment and faster cognitive decline. The authors say this supports using p-tau217 in prognostic models and future trial design.
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67/100
Alzheimer's disease and coronary artery disease are common late-life chronic conditions and share multiple risk factors, including the apolipoprotein E (APOE) ε4 allele.
Why it matters
In the FINGER trial, a two-year multidomain lifestyle intervention improved cognition slightly more in people with higher genetic risk scores for Alzheimer's disease or coronary artery disease. The genetic risk scores themselves were not significantly related to cognition, and the analysis was exploratory.
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Understanding the neuropathological effects of amyloid β (Aβ)-targeting therapies and amyloid-related imaging abnormalities (ARIA) in Alzheimer's disease is critical for optimising treatment efficacy and patient outcomes.
Why it matters
This retrospective case-control study compared clinicopathological changes and amyloid-related imaging abnormalities in five aducanumab-treated participants versus untreated Alzheimer's disease, using autopsy and Aβ PET imaging. It examines the neuropathological effects of treatment in a very small sample rather than showing a cure or prevention.
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Down syndrome (DS) is a genetic form of Alzheimer's disease (AD) that offers crucial insights into AD pathogenesis.
Why it matters
This 10-year cohort of 1135 participants found that progression to symptomatic Alzheimer's disease before age 40 was rare in Down syndrome but rates increased after age 50, with a predictable sequence of biomarker changes. It is an observational cohort that supports clinical trials but does not itself provide a treatment or cure.
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We sent invitations to 91,433 households; 5542 (6.1%) responded, 2120 completed the Baseline Survey (78.5% online; 21.5% via computer-assisted telephone interview), and 2087 were deemed eligible, yielding a response rate of 2.3%.
Why it matters
This paper describes the design and recruitment for a trial of APOE genotype disclosure in an urban Latino population, with a response rate of 2.3%. It reports no treatment or prevention outcomes, only that the findings may help develop culturally sensitive educational materials and genetic counseling protocols.
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Among community-dwelling adults included in this study, higher fragmentation of the 24-hour activity rhythms was associated with greater subsequent Aβ burden, especially in APOE4 carriers.
Why it matters
In community-dwelling older adults, more fragmented 24-hour activity rhythms at baseline were associated with greater amyloid burden at follow-up, especially in APOE4 carriers, while no other sleep measure was associated with amyloid. This suggests that rest-activity fragmentation could be a modifiable risk factor for Alzheimer's disease, though the study is observational and cannot prove cause and effect.
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Across the brain, people with Down syndrome had greater concentrations of tau for a given level of amyloid compared with people with autosomal-dominant Alzheimer's disease.
Why it matters
Comparing people with Down syndrome and people with autosomal-dominant Alzheimer's disease, those with Down syndrome had greater tau concentrations for a given amyloid level, and tau increases were more strongly associated with amyloid increases. The general progression of amyloid followed by tau was similar in both groups, but there were subtle differences in the spatial distribution, timing, and magnitude of tau burden.
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67/100
Data from 3960 MRI sessions among 1141 participants were included: 252 pathogenic variant carriers from DIAN (mean [SD] age, 38.4 [11.2] years; 137 [54%] female), 571 older adults from ADNI (mean [SD] age, 72.8 [7.3] years; 274 [48%] female), and 318 older adults from HABS (mean [SD] age, 72.4 [7.6] years; 194 [61%] female).
Why it matters
This large cohort study examined whether white matter hyperintensities in the brain are related to Alzheimer's disease processes themselves or to vascular risk factors. It is an observational study about what causes these brain changes and does not test any treatment.
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Innovations associated with the bayesian approach can improve the efficiency of drug development and the accuracy of clinical trials, even in the context of substantial data missingness.
Why it matters
This Bayesian analysis of a phase 2b trial of lecanemab reports on how the adaptive design improved trial efficiency, not on whether the drug benefits patients. It provides no conclusion about treating, curing, or preventing Alzheimer's disease.
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Most neuroinflammatory CSF biomarkers were associated with WML in individuals without dementia.
Why it matters
In 495 cognitively unimpaired older adults and 247 people with mild cognitive impairment, higher levels of several inflammation-related proteins in spinal fluid went with more white matter lesions on brain scans. More markers were linked in the MCI group (PlGF, IL-16, IL-8, IL-6, VEGF-A, VEGF-D) than in the unimpaired group, where PlGF and IL-8 were reported. Only PlGF stayed linked to lesions regardless of amyloid status and cognitive impairment. These are associations, not causes, and the study tests no treatment.
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67/100
Cox regression and accelerated failure time models were used to investigate whether sex, apolipoprotein E genotype and e4 carriage were associated with amyloid onset age in all cohorts.
Why it matters
This study modelled amyloid onset age from PET imaging and found that apolipoprotein E e4 carriers became amyloid positive at an earlier age, with greater e4 dosage linked to earlier onset. It also found that e4 carriage, being female, and later amyloid onset age were associated with a shorter time from amyloid onset to impairment, but it did not test any treatment.
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We tested the trained model using five other studies, three of which used PET as a biomarker of significant amyloid β burden (testing the deep learning model between amyloid β positive vs amyloid β negative).
Why it matters
This retrospective case-control study tested a deep learning model using retinal photographs to detect Alzheimer's disease, with improved performance in patients with eye disease or diabetes. It is a diagnostic study and does not address treating, curing, or preventing Alzheimer's disease.
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In AD a clinical recommendation can be made for NEURO-AD TM system and for high-frequency rTMS over the left dorsolateral prefrontal cortex (DLPFC) as probably effective protocols (B-level of evidence) and for anodal tDCS over the left DLPFC as a possibly effective.
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.
- Microglial mechanisms drive amyloid-β clearance in immunized patients with Alzheimer's disease
- Longitudinal cognitive decline is associated with fibrillar amyloid-beta measured by [11C]PiB
- The projected effect of risk factor reduction on Alzheimer's disease prevalence
- Consensus meta-analysis of genome-wide association studies for Alzheimer's disease and related dementias
- Circulating levels of IL-1 family cytokines and receptors in Alzheimer's disease: new markers of disease progression?
- Current Role for Biomarkers in Clinical Diagnosis of Alzheimer Disease and Frontotemporal Dementia
- A community-based exercise programme to improve functional ability in people with Alzheimer's disease: a randomized controlled trial
- Gut Microbiota Changes and Their Correlation with Cognitive and Neuropsychiatric Symptoms in Alzheimer's Disease
- The presence of sodium dodecyl sulphate-stable Abeta dimers is strongly associated with Alzheimer-type dementia
- Inhibitory interneuron deficit links altered network activity and cognitive dysfunction in Alzheimer model