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 5,413 studies, highest score first: BibTeX (.bib) · RIS (.ris)
Highest usefulness score first. Studies without a score come last.
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In this study, clinically normal adults with SNAP did not exhibit evidence of elevated tau levels, which suggests that this biomarker construct does not represent amyloid-independent tauopathy.
Why it matters
Among 247 clinically normal older adults, 64 (25.9%) were classified as having SNAP (suspected non-Alzheimer disease pathophysiology). Their tau levels in the temporal lobes were indistinguishable from the stage 0 group and lower than the stage 2 group, and the stage 2 group showed greater cognitive decline than all other groups, while the SNAP group showed a smaller practice effect over time than stage 0; the authors conclude that SNAP does not represent amyloid-independent tauopathy.
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We postulated that cerebral amyloid angiopathy (CAA), characterised by cortical vascular amyloid deposits, is associated with cortical tissue loss independent of parenchymal Alzheimer's disease pathology.
Why it matters
This case-control study tested whether cerebral amyloid angiopathy is linked to loss of cortical grey matter independent of Alzheimer's disease pathology. It is observational and does not test any treatment or cure.
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Autosomal-dominant AD is associated with increased WMH well before expected symptom onset.
Why it matters
Among 299 adults from families with inherited Alzheimer's disease, people carrying a causal mutation had more white matter hyperintensities on MRI (brain changes that usually reflect small-vessel disease) than their non-carrier relatives. The difference appeared about 6 years before their estimated symptom onset, and in the parietal and occipital lobes as early as 22 years before. The authors say this suggests the possibility that these changes are a core part of Alzheimer's rather than only a separate vascular add-on; the study used one baseline scan per person, and it reports no effect sizes and does not test whether the finding applies to common late-onset Alzheimer's.
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More research is needed to elucidate the neural mechanisms underlying these regional associations, which may involve motor and sensorimotor circuits hitherto largely neglected in the pathophysiology of AD.
Why it matters
In 128 older adults at high risk for dementia, nearly all with memory complaints, those with more amyloid on PET scans in the putamen, occipital cortex, precuneus and anterior cingulate walked more slowly over 4 meters, after adjusting for age, sex, education, BMI and APOE genotype. The authors say this confirms in living people earlier postmortem evidence linking Alzheimer's pathology to gait speed. Because everyone was measured once, it shows a link, not that amyloid causes slower walking; the mechanisms remain unknown.
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Patients with AD and individuals at risk for AD show reduced glucose metabolism, as indexed by fludeoxyglucose F 18-labeled positron emission tomography (FDG-PET).
Why it matters
This cross-sectional study examined whether insulin resistance predicts Alzheimer-like glucose metabolism deficits in late middle-aged adults at risk for Alzheimer's disease. It does not test any treatment or prevention, so it cannot show whether addressing insulin resistance would change the course of the disease.
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63/100
Overall, memory worsened from age 30 years through the 90s. The HVa worsened gradually from age 30 years to the mid-60s and more steeply beyond that age.
Why it matters
In 1,246 cognitively normal people aged 30 to 95, all measured at one point in time at a single academic center, those in older age groups had poorer memory and smaller hippocampi, starting decades before the ages at which amyloid on PET scans rose (the median stayed low until about 70). Men had poorer memory and smaller hippocampi than women but no difference in amyloid, while APOE ε4 carriers had more amyloid from age 70 onward but not poorer memory or smaller hippocampi. The authors conclude that something other than amyloid drives memory and brain-structure decline in middle age; this compares age groups rather than following people over time, and it does not test any treatment.
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By conditioning on the genetic association with the cardiovascular phenotypes, we identify novel AD susceptibility loci, including 2 genome-wide significant variants conferring increased risk for AD.
Why it matters
Genetic variants linked to Alzheimer's disease were found to overlap with variants linked to C-reactive protein and plasma lipids such as LDL, HDL, and triglycerides. By accounting for this shared genetic signal, the researchers identified new Alzheimer's susceptibility loci, including two genome-wide significant variants.
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Their 3-year progression rate to Alzheimer's disease-type dementia was 50% compared to 21% for subjects without prodromal Alzheimer's disease.
Why it matters
In this study, people with prodromal Alzheimer's disease at the mild cognitive impairment stage had 3-year progression rates to Alzheimer's disease-type dementia of 50% and 61%, compared with 21% and 22% in those without prodromal Alzheimer's disease. The findings support using the proposed research criteria to identify Alzheimer's disease at the mild cognitive impairment stage, which may help identify people for future treatment studies.
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Cross-sectional functional magnetic resonance imaging studies using a memory task in patients with mild cognitive impairment have produced discordant results, with some studies reporting increased hippocampal activity--consistent with findings in genetic at-risk populations--and other studies reporting decreased hippocampal activity, relative to normal controls.
Why it matters
In 33 patients with mild cognitive impairment, those who were amyloid-β positive showed increased hippocampal activation, smaller hippocampal volumes, and a trend towards lower Mini-Mental State Examination scores at baseline. The study examined how amyloid-β deposition relates to brain activity, atrophy and clinical progression, and did not test any treatment.
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We investigated induction of α-secretase A disintegrin and metalloprotease 10 (ADAM10) by the synthetic retinoid acitretin (Neotigason; Actavis, München-Riem, Germany) in patients with mild to moderate Alzheimer disease (AD) via measurement of CSF content of α-secretase-derived amyloid precursor protein (APPs-α).
Why it matters
In a 4-week double-blind study of 21 patients with mild to moderate Alzheimer's disease, acitretin treatment was assessed by measuring CSF APPs-α levels, along with safety and tolerability. This small short trial measured a biomarker and did not show that acitretin treats, cures, or prevents Alzheimer's disease.
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63/100
Researchers analyzed population-based data and relative risks from existing meta-analyses to estimate the population-attributable risk of Alzheimer's disease worldwide, in the USA, Europe, and the UK for seven potentially modifiable risk factors.
Why it matters
An analysis of population-based data on how much Alzheimer's disease might be prevented in the first place. Estimates of this kind describe potential, and do not show that acting on any particular risk factor prevents the disease.
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This study shows significant therapeutic effects of trazodone 50 mg in community-dwelling AD patients with SD.
Why it matters
In this small 2-week trial, trazodone increased nighttime sleep in people with Alzheimer disease and sleep disturbances, without affecting cognition or daytime sleepiness. This suggests trazodone may help with sleep problems but does not treat the disease itself.
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Previous studies from our group have shown that language changes may be reflected in connected speech production in the earliest stages of typical Alzheimer's disease.
Why it matters
This study examined connected speech as a marker of disease progression in people with autopsy-proven Alzheimer's disease. It found that subtle language changes were evident in the prodromal stages and showed linear trends over disease stages, but it is about tracking progression, not treatment or cure.
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63/100
Partial volume corrected and uncorrected results were generally in agreement; however, the correlation between (11)C-PBR28 and (11)C-Pittsburgh Compound B binding was seen only after partial volume correction.
Why it matters
The results suggest that neuroinflammation, shown by increased binding to TSPO, occurs after conversion of mild cognitive impairment to Alzheimer's disease and worsens as the disease progresses. This points to inflammation as a process tied to disease progression rather than its earliest stage.
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Although it is clear that astrocytes and microglia cluster around dense-core amyloid plaques in Alzheimer disease (AD), whether they are primarily attracted to amyloid deposits or are just reacting to plaque-associated neuritic damage remains elusive.
Why it matters
This study examined brain tissue from 40 Alzheimer's patients and found that both astrocytes and microglia cluster around dense-core amyloid plaques, with different patterns of response. It describes brain pathology but does not test or report any treatment, cure, or prevention for Alzheimer's disease.
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The data are consistent with expected rates of amyloid positivity among individuals with clinical diagnoses of AD and MCI, and indicate the potential value of florbetapir F18 PET as an adjunct to clinical diagnosis.
Why it matters
In 184 people, florbetapir PET detected amyloid in 76% of Alzheimer patients, 38% of those with mild cognitive impairment and 14% of healthy controls. This supports the scan as an aid to clinical diagnosis, not as a treatment, cure or prevention.
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At baseline measurements, amyloid burden does not distinguish between cognitively impaired and unimpaired subjects with PD without dementia, but our data suggest that amyloid contributes to cognitive, but not motor, decline over time.
Why it matters
In this small cohort of 46 people with Parkinson disease without dementia, baseline amyloid burden did not distinguish those with mild cognitive impairment from those with normal cognition, but higher amyloid retention predicted conversion to a more severe diagnosis. It is an early observational finding in Parkinson disease and does not test a treatment, cure, or prevention for Alzheimer's disease.
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44 participants were included: 20 PSEN1 E280A mutation carriers and 24 non-carriers.
Why it matters
In 44 Colombians aged 18–26 from one family (20 carrying the PSEN1 E280A mutation, which causes early-onset Alzheimer's disease, and 24 non-carriers), carriers showed brain-scan and spinal-fluid/blood differences that the authors describe as "consistent with Aβ(1-42) overproduction," including greater right hippocampal and parahippocampal activation during a memory task, even though the two groups did not differ on dementia ratings or thinking tests. The authors call these "the earliest known biomarker changes in cognitively normal people" at genetic risk for this inherited form of Alzheimer's, but say it is still undetermined whether the changes are "neurodegenerative or developmental." It is a single-timepoint comparison in one mutation-carrying family and tested no treatment.
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This study provides initial data that demonstrate elevated antibodies to periodontal disease bacteria in subjects years before cognitive impairment and suggests that periodontal disease could potentially contribute to the risk of AD onset/progression.
Why it matters
In 158 people who were cognitively intact at the start, higher serum antibody levels to the periodontal bacterium Fusobacterium nucleatum were found in those who later developed Alzheimer's disease or mild cognitive impairment. This links a marker of periodontal infection to later cognitive decline, but it does not show that treating gum disease would prevent or cure Alzheimer's disease.
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A consensus panel from the United States and Europe was convened recently to update and revise the 1997 consensus guidelines for the neuropathologic evaluation of Alzheimer's disease (AD) and other diseases of brain that are common in the elderly.
Why it matters
A US–European consensus panel revised the 1997 guidelines for examining the brain after death for Alzheimer's disease. The update recognises a "pre-clinical stage" of the disease and assesses amyloid build-up as well as neurofibrillary change and neuritic plaques. It also sets protocols for Lewy body disease, vascular brain injury, hippocampal sclerosis and TDP-43 inclusions, and recommends standard ways to compare brain findings with a person's symptoms in life. These are standards for pathologists and researchers, not a test, treatment or prevention.
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Naproxen may attenuate cognitive decline in slow decliners while accelerating decline in fast decliners.
Why it matters
This re-analysis of 2,388 participants in the Alzheimer's Disease Anti-inflammatory Prevention Trial used how fast people's 3MS cognitive test scores fell as a stand-in for how far pre-clinical Alzheimer's had progressed, and found three groups: no, slow and fast decline. The authors report that naproxen "may attenuate cognitive decline in slow decliners while accelerating decline in fast decliners," while celecoxib "appeared to have similar effects at first but then attenuated change in fast decliners." They call these contrasts "unexpected," so the study suggests that drug effects may differ by disease phase; it does not show that anti-inflammatory drugs protect against Alzheimer's.
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Recent GWAS studies focused on uncovering novel genetic loci related to AD have revealed associations with variants near CLU, CR1, PICALM and BIN1.
Why it matters
This genome-wide association study in 1034 cases and 1186 controls, combined with other datasets, replicated associations near PICALM and CR1 and identified variants at the BIN1 locus linked to late-onset Alzheimer's disease. It identifies genetic risk factors but does not provide a treatment, cure or prevention.
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Aβ deposition increases slowly from cognitive normality to moderate severity DAT.
Why it matters
In 206 people (35 with Alzheimer's dementia, 65 with mild cognitive impairment, 106 healthy controls) given repeat amyloid PET scans about 20 months apart, amyloid rose slightly in the dementia and MCI groups and in healthy people who already had high amyloid, and the rise was associated with the number of APOE ε4 alleles. People with mild cognitive impairment and high amyloid progressed to Alzheimer's dementia far more often than those with low amyloid (67% vs 5%), and 25% of healthy controls with high amyloid developed impairment by 3 years. But the link between rising amyloid and cognitive decline was weak, and 20% of low-amyloid MCI patients developed other dementias, so a scan result is a risk signal, not a diagnosis. The study describes no treatment.
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Poor vitamin D nutrition is linked with dementia, but vitamin D has not been tested in a randomized controlled trial (RCT) in Alzheimer's disease (AD).
Why it matters
This small randomized trial gave high-dose vitamin D followed by nasal insulin to 32 people with mild to moderate Alzheimer's disease. It does not report that this combination prevents or cures Alzheimer's disease.
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We used a new method of pooling cerebrospinal fluid Aβ42 and Pittsburgh compound B positron emission tomography measures to produce equivalent measures of brain Aβ load from either source and analysed the results using multiple imputation methods.
Why it matters
Among people with mild cognitive impairment, those who tested amyloid-positive (by spinal-fluid test or PET scan, pooled onto one scale) were much more likely to progress to dementia within 2 years than those who tested negative — 50% versus 19%. Above high levels, having more amyloid did not further raise the risk, which the authors say is "consistent with" amyloid starting the disease process rather than directly causing the memory and thinking problems. This is a prediction study, not a treatment study, and although the title also names MRI atrophy as a predictor, the summary gives no MRI result.
From across this topic
10 of the 5,374 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.
- Design and first baseline data of the DZNE multicenter observational study on predementia Alzheimer's disease (DELCODE)
- Characterize demographics, comorbidities and co‐medications in newly diagnosed United States (US) Alzheimer’s Disease patients using Medicare claims
- Amyloid-β PET-Correlation with cerebrospinal fluid biomarkers and prediction of Alzheimer´s disease diagnosis in a memory clinic
- Homocysteine and holotranscobalamin and the risk of Alzheimer disease: a longitudinal study
- Machine Learning Models of Polygenic Risk for Enhanced Prediction of Alzheimer Disease Endophenotypes
- Default-mode network activity distinguishes Alzheimer's disease from healthy aging: Evidence from functional MRI
- COVID-19 and Alzheimer's disease: how one crisis worsens the other
- Role of RAGE in Alzheimer's Disease
- Survival and mortality differences between dementia with Lewy bodies vs Alzheimer disease
- A new rating scale for Alzheimer's disease