Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.
Download bibliography of all 5,209 studies, highest score first: BibTeX (.bib) · RIS (.ris)
Highest usefulness score first. Studies without a score come last.
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20 participants--15 in the AN1792 group, five in the placebo group--died before follow-up started.
Why it matters
This follow-up of a vaccine trial found that although immunisation could clear amyloid plaques, there was no evidence of improved survival or of a delay in time to severe dementia compared with placebo. The results do not support this immunisation as a treatment that changes the course of Alzheimer's disease.
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One hundred seventy-four patients fulfilled the trial.
Why it matters
In this randomized, double-blind trial, 204 people with mild to moderate Alzheimer's who were already stable on a cholinesterase-inhibitor drug took either omega-3 (1.7 g DHA plus 0.6 g EPA daily) or placebo for 6 months; 174 completed it. Decline on the MMSE and ADAS-cog "did not differ between the groups", so omega-3 did not slow cognitive decline overall. The authors report "positive effects" only in a small group of 32 people with very mild Alzheimer's (MMSE above 27), a finding that needs confirmation rather than one to act on.
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71/100
LY450139 dihydrate, a gamma-secretase inhibitor, was studied in a randomized, controlled trial of 70 patients with Alzheimer disease.
Why it matters
The gamma-secretase inhibitor LY450139 lowered Abeta(1-40) in plasma by 38.2%, but the decrease in cerebrospinal fluid was not significant. The authors suggest higher drug doses may be needed to produce a measurable decrease in CSF Abeta.
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Studies of automobile accident frequency among drivers with AD have yielded conflicting results about the risk of accidents.
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71/100
Metrifonate was safe and well-tolerated.
Why it matters
In this 26-week double-blind trial, the acetylcholinesterase inhibitor metrifonate produced a 2.86-point treatment difference on the ADAS-Cog and differences on global and behavioral measures in patients with mild to moderate Alzheimer's disease. It addresses symptom benefit only and does not show that metrifonate cures or prevents the disease.
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Predicting not just if, but also when, cognitively unimpaired individuals are likely to develop onset of Alzheimer's disease (AD) symptoms would be useful to clinical trials and, eventually, clinical practice.
Why it matters
Using repeated blood tests for a tau marker, this study estimated the age at which a person would first test positive and linked it to the age when Alzheimer's symptoms began, with a median error of about 3 to 3.7 years. The authors suggest this single blood test approach could be useful for clinical trials, though it is not yet a clinical tool.
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Sixty consecutive patients with prodromal or mild AD were screened; 50 were randomized to gamma or sham tACS (mean [SD] age, 67.3 [7.8] years; 25 [50.0%] female and 25 [50.0%] male).
Why it matters
In 50 patients with prodromal or mild Alzheimer's disease, home-based gamma transcranial alternating current stimulation was linked to better scores on global cognition, daily living and associative memory than sham. The authors say these findings support further investigation, so this is not yet an established treatment or cure.
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Of 4467 participants who underwent 9208 longitudinal cognitive sessions, 2698 (60.4%) were female, and the mean age (SD) was 74.3 (9.2) years; 3213 were cognitively unimpaired, 972 had mild cognitive impairment, and 282 had AD dementia.
Why it matters
The study highlights the importance of free-water correction in diffusion MRI and points to the limbic system, especially the cingulum and fornix, as key regions associated with cognitive decline. It is about imaging markers of neurodegeneration, not about treating, curing, or preventing Alzheimer's disease.
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In DDI (n = 431), participants were classified as CN A-/T- (n = 169), A+/T- (CN = 26, MCI = 24), A+/T+ (CN = 40, MCI = 105), and A-/T+ (CN = 34, MCI = 33), with a mean age of 64.1 years and 55.9% female.
Why it matters
In predementia Alzheimer's, plasma p-tau217 aligned well with amyloid status and memory decline, while p-tau181 and p-tau231 did not align as consistently. This is about improving diagnosis and prognosis with biomarkers, not about treating, curing, or preventing Alzheimer's.
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However, the importance of detailed cognitive phenotyping in patients without dementia when interpreting p-tau217 results remains unclear.
Why it matters
In two clinical cohorts, the prevalence of amyloid varied across cognitive phenotypes and this was associated with how well blood p-tau217 models detected brain amyloid. This concerns how to interpret a blood test, not a treatment, cure or prevention.
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We analyzed 1,240 MRIs from 473 patients (age: 69.2 ± 7.4 [range: 49-87]; 32.8% women).
Why it matters
In 473 patients with neurodegenerative or cerebrovascular diseases followed for 2 years, elevated baseline GFAP, NfL, p-tau181, and p-tau217 were associated with more brain atrophy and white matter hyperintensity burden. This is an observational biomarker-imaging study and does not test any treatment, cure, or prevention for Alzheimer's disease.
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US clinical practice guidelines for the diagnostic evaluation of cognitive impairment due to Alzheimer's disease (AD) or AD and related dementias (ADRD) are decades old and aimed at specialists.
Why it matters
This guideline aims to help all clinicians, including primary care, use a structured approach to evaluate patients with symptoms that may represent Alzheimer's disease or related dementias. The authors say that if clinicians use the guideline and health-care systems provide adequate resources, outcomes should improve in most patients in most practice settings.
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In the discovery cohort, the mean (SD) age was 70.9 (8.5) years, 191 (58%) were male, the mean (SD) MMSE score was 27.1 (1.9), and 110 individuals with MCI (33%) converted to dementia (71 to AD dementia).
Why it matters
In people with mild cognitive impairment, tau PET was the best single imaging marker for predicting who would progress to dementia. This is about prognosis and prediction, not about a treatment or cure for Alzheimer's disease.
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Of 6256 participants (3402 women [54.4%]; mean [SD] age at baseline, 61.7 [6.6] years), 510 received an all-cause dementia diagnosis within 17 years of baseline.
Why it matters
In this cohort, impaired kidney function at baseline was not associated with a higher risk of all-cause dementia, Alzheimer disease, or vascular dementia over 17 years. It found no significant effect on dementia risk and does not test any treatment, cure, or prevention.
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Overall, 2,277 individuals had at least 1 baseline blood biomarker available (n = 357 for CSF subsample, n = 649 for PET subsample), among whom 257 were diagnosed with clinical AD/mixed dementia during follow-up.
Why it matters
In this clinic-based cohort of people with subjective cognitive complaint or mild cognitive impairment, blood biomarkers were only mildly correlated with their equivalents in cerebrospinal fluid. The authors state that these blood biomarkers may be good hallmarks of underlying pathology but add little to clinical prediction of dementia risk.
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These findings suggest that this blood biomarker test could allow for distinguishing individuals with brain amyloid-positive PET findings from individuals with amyloid-negative PET findings and serve as an aid for Alzheimer disease diagnosis.
Why it matters
In 686 participants with mild cognitive impairment or mild dementia, a model combining plasma Aβ42:40 ratio, apoE proteotype and age distinguished people with amyloid-positive PET findings from those with amyloid-negative findings. This is a blood test to aid diagnosis, not a treatment, cure or prevention.
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This study found that CSF-based estimates using adjusted data-driven cutoffs were up to 10% higher than PET-based estimates in people without dementia, whereas the results were similar among people with dementia.
Why it matters
CSF-based estimates of amyloid abnormality were up to 10% higher than PET-based estimates in people without dementia, suggesting preclinical and prodromal Alzheimer's disease may be more common than previously estimated. This affects trial recruitment and health care planning, not treatment or cure.
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70/100
Common genetic variance in apolipoprotein E (APOE), β-glucocerebrosidase (GBA), microtubule-associated protein tau (MAPT), and α-synuclein (SNCA) has been linked to cognitive decline in Parkinson's disease (PD), although studies have yielded mixed results.
Why it matters
This pooled analysis of six population-based cohorts genotyped 1002 patients with newly diagnosed Parkinson's disease for APOE, GBA, MAPT, and SNCA variants and followed them for up to 10 years to assess cognitive decline and dementia risk. It examines genetic influences on cognitive decline in Parkinson's disease and does not test any treatment, cure, or prevention.
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This is the first randomized trial to investigate the impact of a ketogenic diet in patients with uniform diagnoses of AD.
Why it matters
In this small 12-week trial of 26 patients, a modified ketogenic diet improved daily function and quality of life scores, but the change in cognition was not significant. These are short-term results in a small sample and do not show that the diet treats, cures, or prevents Alzheimer's disease.
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Therefore, we conducted a longitudinal study to examine whether PM2.5 affects the episodic memory decline, and also explored the potential mediating role of increased neuroanatomic risk of Alzheimer's disease associated with exposure.
Why it matters
Long-term exposure to fine particulate air pollution was linked to faster decline in some immediate memory and new learning measures, but not in delayed recall or composite scores, and part of this effect appeared to go through brain atrophy linked to Alzheimer's disease risk. This is an observational study and does not show that reducing pollution prevents or treats Alzheimer's disease.
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Parietal cortex RNA-sequencing (RNA-seq) data were generated from individuals with and without Alzheimer disease (AD; n control = 13; n AD = 83) from the Knight Alzheimer Disease Research Center (Knight ADRC).
Why it matters
This study found associations between circular RNA expression and Alzheimer's disease diagnosis, dementia severity, and neuropathological severity, with some changes appearing early in presymptomatic disease. It is a tissue and data analysis that supports future studies of circular RNAs in Alzheimer's disease; it does not test any treatment.
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These were compared with the prevalence of 3 clinically defined diagnostic groups (mild cognitive impairment or dementia, dementia, and clinically defined probable Alzheimer disease).
Why it matters
Biologically defined Alzheimer's disease was more prevalent than clinically defined probable Alzheimer's disease at any age and three times more prevalent at age 85. This has implications for public health planning and for intervening with disease-specific treatments to prevent symptom onset, but the study itself tested no treatment.
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APOE ε4 may influence the association between WMH and cognitive performance in AD and DLB.
Why it matters
Greater white matter hyperintensity volume was associated with worse attention/executive functions, learning/memory and language only in APOE ε4 carriers, with no significant associations in noncarriers. This describes how a genetic factor and vascular brain changes relate to cognition, not a treatment, cure or prevention for Alzheimer's disease.
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Analyses measured the associations between predictor variables and the memory score, and whether AT(N) biomarker profiles significantly improved prediction of memory z score rates of change beyond a model with clinical and genetic variables only.
Why it matters
Adding amyloid PET, tau PET and MRI cortical thickness gave only a small but statistically significant improvement in predicting memory decline over clinical and genetic information alone. It is a prediction tool, not a treatment or cure.
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Alzheimer's dementia is significantly more common in women than in men.
Why it matters
This study used post-mortem data from 1,453 participants in two community-based studies to examine sex differences in Alzheimer's disease and other brain pathologies. It is a pathological description and does not report a 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.
- Divergent social functioning in behavioral variant frontotemporal dementia and Alzheimer disease: reciprocal networks and neuronal evolution
- Safety and tolerability of the γ-secretase inhibitor avagacestat in a phase 2 study of mild to moderate Alzheimer disease
- Plasma Phosphorylated Tau 217 and Amyloid Burden in Older Adults Without Cognitive Impairment: A Meta-Analysis
- Neuroimaging correlates of pathologically defined subtypes of Alzheimer's disease: a case-control study
- Automated 3D mapping of hippocampal atrophy and its clinical correlates in 400 subjects with Alzheimer's disease, mild cognitive impairment, and elderly controls
- Amyloid PET Quantification Via End-to-End Training of a Deep Learning
- Prognostic value of plasma glial fibrillary acidic protein in cognitively unimpaired older adults: Results from the A4 study
- Music therapy and Alzheimer's disease: Cognitive, psychological, and behavioural effects
- Machine learning based hierarchical classification of frontotemporal dementia and Alzheimer's disease
- Network pharmacology-based analysis of Chinese herbal Naodesheng formula for application to Alzheimer's disease