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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Low baseline Aβ42/Aβ40 was significantly associated with increased amyloid accumulation (β = 0.257, 95% confidence interval (CI) 0.177-0.336, P < 0.001), and with higher risk of conversion to Aβ-PET positivity (Hazard ratio (HR) = 2.84, 95% CI 1.14-7.04, P = 0.025) and to MCI due to AD (HR = 3.25, 95% CI 1.17-9.01, P = 0.024).
Why it matters
This longitudinal study found that low plasma Aβ42/Aβ40 was associated with increased amyloid accumulation, brain atrophy, and conversion to mild cognitive impairment due to Alzheimer's disease in people with subjective cognitive decline. It suggests the biomarker may help identify those at higher risk of progression but does not test any treatment, cure, or prevention.
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Alzheimer\\\'s disease (AD), the leading cause of dementia worldwide, affects more than 55 million individuals and gen-erates annual healthcare costs exceeding two trillion USD [14].
Why it matters
A reviewed longitudinal MRI study using 3D CNNs, T-LSTM networks, and radiomics predicted MCI-to-AD conversion with a c-index of 0.90 and time-specific AUCs of 0.96, 0.94, and 0.89 for 2-, 3-, and 5-year prediction. This is a prediction and prognostication tool, not a treatment, cure, or prevention.
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Functional impairment (FI) is a key criterion for diagnosing dementia.
Why it matters
This study examined how persistent versus transient functional impairment relates to CSF Alzheimer's biomarkers and later dementia in dementia-free older adults. It addresses early detection and progression, not treatment, cure or prevention.
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ATTRACTnet was developed in an internal test set of 799 patients (mean [SD] age, 75.1 [11.1] years; 516 [64.7%] male and 283 [35.3%] female) using 5-fold cross-validation with an additional external test set of 422 patients.
Why it matters
An artificial intelligence model detected transthyretin cardiac amyloidosis with good discrimination, and among tested patients, 24 of 50 were diagnosed and 21 started treatment within three months. This concerns heart amyloidosis detection, not treating, curing, or preventing Alzheimer's disease, and the authors say randomized trials are needed to show whether outcomes improve.
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55/100
BackgroundWhile cortical atrophy has been widely studied in dementia, emerging evidence highlights the role of subcortical degeneration, particularly in deep gray matter structures such as the thalamus, claustrum, and basal nuclei, in both Alzheimer's disease (AD) and frontotemporal dementia (FTD).
Why it matters
Deep gray matter structures such as the thalamus, nucleus accumbens, and claustrum showed atrophy in both Alzheimer's disease and frontotemporal dementia, with greater and faster atrophy in behavioral variant frontotemporal dementia. A classification model distinguished the diseases with high accuracy, which is relevant to diagnosis rather than treatment.
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PD may be a modifiable risk factor for AD, and periodontal interventions could contribute to AD prevention and management.
Why it matters
This scoping review pulled together 52 studies on gum (periodontal) disease and Alzheimer's, including 25 clinical studies of the link. The evidence suggests gum disease raises Alzheimer's risk and speeds cognitive decline, possibly through inflammation driven by the mouth bacterium Porphyromonas gingivalis. The authors call gum disease a possibly modifiable risk factor, but say more clinical studies are needed before gum treatment can be counted on to help prevent Alzheimer's.
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< 0.001). Stage-specific tau-PET region-of-interest selection reduced required sample sizes by 30%-93% for detecting hypothetical disease-modifying drug effects.
Why it matters
Selecting tau-PET regions based on biological disease stage reduced the sample sizes needed to detect hypothetical drug effects by 30% to 93%. This is a trial-design finding and does not show that any treatment works.
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AD exhibited elevated serum GFAP levels in comparison to control patients (P < 0.0001).
Why it matters
Serum GFAP was elevated in Alzheimer's disease compared with controls, and age-corrected z-scores and cut-offs were developed, with better diagnostic performance in early-onset than elderly groups. This is a diagnostic tool and does not address treating, curing or preventing the disease.
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Based on data from their first NACC visit with AD, there was considerable heterogeneity in language performance across people with EOAD and LOAD.
Why it matters
Using data from first NACC visits, this study found that people with late-onset Alzheimer's disease dementia performed better on average than those with early-onset disease in category fluency, letter fluency and spoken lexical retrieval, with no significant group difference in confrontation naming. It describes differences in language profiles at diagnosis and does not test any treatment, cure or prevention.
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A single-timepoint ResNet3D model achieved modest performance (c-index ~ 0.70).
Why it matters
Deep learning models using longitudinal structural MRI predicted conversion from mild cognitive impairment to Alzheimer's disease with c-index 0.80-0.90, better than a single-timepoint model. The authors note limitations in sample size and computational resources warrant larger, more diverse studies to confirm the findings.
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55/100
The data of 508,107 individuals were analyzed (mean [standard deviation] age, 67.6 [10.7] years; 66.8% women and 33.2% men), and 39,318 developed Alzheimer's disease (22,572 controls and 16,746 using aspirin).
Why it matters
This cohort study found that aspirin use was associated with a reduced risk of conversion from mild cognitive impairment to Alzheimer's disease, but also with an increased risk of hemorrhagic stroke. It suggests a possible association but does not establish that aspirin prevents Alzheimer's disease, and the bleeding risk must be considered.
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55/100
A substantial difference in the type of therapeutics researched was observed, with anti-amyloid and anti-tau RCTs being more likely to be funded by the pharmaceutical industry compared with neurotransmitter or other RCTs (anti-amyloid or anti-tau, 68 of 71 [95.8%]; neurotransmitter, 52 of 69 [77.6%]; other, 33 of 52 [63.5%]).
Why it matters
This study analyzed 203 past Alzheimer's trials and found that anti-amyloid and anti-tau trials were more likely to be funded by the pharmaceutical industry than other types of trials. It does not report whether any treatment worked, only how trial funding and design have changed over time.
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Individuals with Down syndrome (DS) have a genetically determined form of Alzheimer's disease (AD) due to the amyloid precursor protein (APP) gene dose effect.
Why it matters
This perspective notes that people with Down syndrome, who have a genetically determined form of Alzheimer's disease, were excluded from pivotal trials of anti-amyloid therapies such as lecanemab and donanemab. It highlights gaps in safety and efficacy data for this group rather than reporting a treatment, cure or prevention.
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Of 9,361 SPRINT participants (mean age 67.1 ± 9.5 years, 36.7% female, 58.7% non-Hispanic White), 710 and 1,289 were new users of an ARB or ACEI.
Why it matters
This study found insufficient evidence to conclude that initiating and adhering to an ARB versus an ACEI reduces the risk of mild cognitive impairment or dementia. It did find that ARB use was associated with lower risk of all-cause death compared to ACEI.
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. Longitudinally, older age (OR=1.14 [1.06-1.22], p<.001), higher levels of p-tau217 (OR=10.37 [3.00-35.02], p<.001) and higher neuropsychiatric symptoms (OR=1.19 [1.02-1.39], p=.023) were associated with higher odds of progression to dementia.
Why it matters
In people with mild cognitive impairment, elevated plasma p-tau217 was linked to much higher odds of progressing to dementia, indicating that this blood marker can help define who has Alzheimer's pathology and a worse prognosis. The findings are about prognosis and classification, not about a treatment or cure.
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Portable, low-field magnetic resonance imaging (LF-MRI) of the brain may facilitate point-of-care assessment of patients with Alzheimer's disease (AD) in settings where conventional MRI cannot.
Why it matters
This study optimized portable, low-field MRI acquisition and developed a machine learning pipeline to quantify brain morphometry and white matter hyperintensities in patients with mild cognitive impairment or dementia due to Alzheimer's disease. Hippocampal volumes from these scans agreed with conventional MRI, and the authors suggest this could increase access to neuroimaging for dementia.
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Our results suggest that reactive astrogliosis, as indicated by different fluid biomarkers, influences the pathogenic cascade during the preclinical stage of AD.
Why it matters
In cognitively unimpaired people, this analysis suggested that astrocyte biomarkers GFAP and YKL-40 sit within the chain linking amyloid, tau, and neuronal injury in the earliest stages. This is about how the disease process may unfold, not about treating, curing, or preventing it.
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55/100
As the leading cause of dementia, Alzheimer's disease (AD) is a major burden on affected individuals, their families and caregivers, and healthcare systems.
Why it matters
This review describes plasma phosphorylated tau as a promising blood biomarker that can distinguish Alzheimer's disease from other neurodegenerative diseases and inform diagnosis and eligibility for approved therapies. It is about diagnosis and trial use, not about treating, curing or preventing the disease.
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Blood-based biomarkers offer a major advance in the clinical evaluation of neurodegenerative diseases.
Why it matters
This review describes blood-based biomarkers for amyloid and tau pathology and for neuronal and glial degeneration that may soon be used for screening, diagnosis, or monitoring. It is about biomarkers and does not show that any treatment, cure, or prevention works.
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55/100
The findings do not support an effect of the exercise intervention on a single measure of neurodegeneration in AD.
Why it matters
In 136 patients with mild Alzheimer's disease, a 16-week aerobic exercise program did not reduce serum neurofilament light compared with usual care. The study found no effect of this exercise intervention on this single measure of neurodegeneration.
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We compared digital speech and language features of patients with amnestic Alzheimer disease (aAD) or logopenic variant primary progressive aphasia (lvPPA) in a biologically confirmed cohort and related these features to neuropsychiatric test scores and CSF analytes.
Why it matters
This cross-sectional study compared automated speech and language features in patients with biologically confirmed Alzheimer disease and healthy controls, and related them to test scores and CSF analytes. It is a single-time-point study, so it cannot show whether speech changes predict or respond to treatment.
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Sex or gender differences in the risk of Alzheimer's disease and related dementias (ADRD) differ by world region, suggesting that there are potentially modifiable risk factors for intervention.
Why it matters
This perspective notes that sex and gender differences in Alzheimer's disease and related dementias risk vary by world region, suggesting potentially modifiable risk factors, and that discrimination against women and sex and gender minority populations contributes to cognitive decline. It calls for identifying drivers of these differences as a first step toward tailored interventions, not a proven treatment.
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Anodal tDCS+CS delays cognitive decline (ADAS-cog change) to a greater extent than sham tDCS+CS (-3.4±1.1 vs. -1.7±0.4; p=.03).
Why it matters
In this trial, people with Alzheimer disease who received active transcranial direct current stimulation combined with cognitive stimulation showed less cognitive decline than those who received sham stimulation. This is a small trial, and it tested a symptomatic treatment rather than a cure or prevention.
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Alzheimer's disease (AD) is prevalent throughout the world and is the leading cause of dementia in older individuals (aged ≥ 65 years).
Why it matters
A review of 2014–2021 PubMed literature from North America, Europe and Asia reports that, among people with mild cognitive impairment, Alzheimer's is estimated to be the cause in 40% to 75% of cases, "depending on the populations studied and whether the MCI diagnosis was made clinically or in combination with biomarkers." For people with both amyloid buildup and neurodegeneration, it cites lifetime risk of Alzheimer's dementia estimated at 41.9% for women and 33.6% for men, while noting that data on the earliest, preclinical stage are sparse. The authors expect biomarkers used alongside cognitive tests to become an important part of clinical practice as new disease-modifying therapies arrive.
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Cerebrospinal fluid (CSF) tau and beta-amyloid levels in chronic traumatic encephalopathy (CTE), a disease which can be clinically indistinguishable from Alzheimer's disease (AD), are largely unknown.
Why it matters
This cross-sectional study compared cerebrospinal fluid tau and beta-amyloid levels in people with autopsy-confirmed chronic traumatic encephalopathy and Alzheimer's disease. It is a diagnostic comparison and does not test any treatment, cure or prevention.
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.
- Salvia officinalis extract in the treatment of patients with mild to moderate Alzheimer's disease: a double blind, randomized and placebo-controlled trial
- Plasma GFAP outperforms CSF GFAP in detecting amyloid pathology and is associated with increased risk of clinical progression in early Alzheimer's disease
- Mendelian randomization study of genetic interactions between Alzheimer disease and celiac disease
- Additive value of early-phase β-Amyloid-PET for the differential diagnosis of non-Alzheimer’s disease dementia
- Feasibility, Safety, and Preliminary Efficacy of Partnered Rhythmic Rehabilitation in Prodromal Alzheimer's Disease: A 12-Month Pilot Randomized Controlled Trial
- Pharmaceutical developments in alzheimer's disease: An emphasis on blarcamesine
- Mood Changes in Cognitively Normal Older Adults are Linked to Alzheimer Disease Biomarker Levels
- Multi-Target Drug Design in Alzheimer's Disease Treatment: Emerging Technologies, Advantages, Challenges, and Limitations
- Plasma Phosphorylated Tau217–A Pivotal Plasma Biomarker for Predicting the Progression of Mild Cognitive Impairment to Alzheimer’s Disease: A Reanalysis of ADNI Data
- [Alzheimer-type dementia and Down syndrome]