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.
-
Experimental evidence suggests that activated microglia induce astrocyte reactivity in neurodegenerative disorders, such as Alzheimer's disease (AD).
Why it matters
Across 101 individuals studied with PET and plasma biomarkers, amyloid-beta pathology was associated with astrocyte reactivity only in the presence of microglial activation, and these effects related to cognitive impairment through tau phosphorylation and aggregation. This describes a pathway linking microglial activation, astrocytes and tau in the disease process, without testing any treatment, cure or prevention.
-
Biomarkers were measured in 431 Black and 583 White participants (mean age of 77 and 80 years and 17% and 21% of men, respectively), generating a balanced sample of 366:366.
Why it matters
In Black and White older adults, plasma pTau217 was strongly linked to dementia risk and cognitive decline. This is a biomarker study for detection and risk assessment, not a treatment or cure.
-
For the intention-to-treat analysis, 60 patients between ages 51 and 82 years (mean [SD], 70.65 [8.16] years; 30 females; 30 males) were included.
Why it matters
In this trial of 60 patients, the main analysis found no significant overall effect of transcranial pulse stimulation, but a significant interaction with age meant only the subgroup aged 70 or younger showed significantly higher cognitive scores after the real treatment. The authors suggest this technique may be a safe and promising add-on therapy for people already receiving standard Alzheimer treatment.
-
We provide evidence for 16 novel AD loci and advocate for more studies using whole genome sequencing-based GWAS of diverse cohorts.
Why it matters
This multi-ancestry genome-wide association study identified 16 new genetic locations linked to Alzheimer disease, using data that included many participants of non-European ancestry. These findings add to understanding of the disease's genetics and argue for more studies in diverse populations, but they do not yet provide a treatment or cure.
-
There were 132 720 unique adults with Down syndrome from 2011 to 2019: 79 578 (53.2%) were male, 17 090 (11.7%) were non-Hispanic Black, 20 777 (15.7%) were Hispanic, 101 120 (68.8%) were non-Hispanic White, and 47 692 (23.3%) had ever had an Alzheimer dementia diagnosis.
Why it matters
In a cohort of 132,720 adults with Down syndrome from 2011 to 2019, 47,692 had ever had an Alzheimer dementia diagnosis, and mean age at onset and age at death differed across racial and ethnic groups. This is a descriptive study of diagnosis and age patterns and does not test any treatment, cure or prevention.
-
Our findings suggest that statins might be associated with a lower risk of incident AD among individuals with the APOE ε4 allele.
Why it matters
In this cohort, statin initiation was associated with a reduced risk of incident clinical Alzheimer's disease compared with nonusers. The association was stronger among participants with the APOE ε4 allele than among those without it.
-
Increasing evidence suggests an association between pro-inflammatory diets and cognitive function.
Why it matters
This study found that a pro-inflammatory diet was associated with higher risk of all-cause dementia and Alzheimer's dementia in a large cohort. It does not show that changing diet prevents dementia, and the results are observational.
-
Longitudinal tau positron emission tomography (PET) is a relevant outcome in clinical trials evaluating disease-modifying therapies in Alzheimer disease (AD).
Why it matters
This study compared group-level and participant-specific brain regions for measuring change in longitudinal tau PET in people across the Alzheimer's disease clinical continuum. It is a methods comparison, so it does not treat, cure, or prevent Alzheimer's disease.
-
Blood biomarkers showed significant longitudinal changes corresponding to cognitive decline, clinical AD, and structural MRI characteristics.
Why it matters
This study found that blood levels of t-tau and Nf-L rose each year in a large group followed for 17 years, and that GFAP rose faster in Black participants than White participants. It only shows how these blood markers change over time and relate to brain scans; it does not test any treatment, cure, or prevention.
-
Plasma phosphorylated tau at threonine 181 (p-tau181), a well-validated marker of Alzheimer disease (AD) pathologic change, could be a more efficient way to diagnose AD than invasive or expensive biomarkers requiring CSF or PET.
Why it matters
This cross-sectional study examined whether plasma p-tau181 is associated with neuropsychiatric symptoms in preclinical and prodromal Alzheimer's disease. It is an observational biomarker study and does not test any treatment, cure, or prevention.
-
Among 580 participants (PREVENT-AD, 128; HABS, 153; AIBL, 48; Knight ADRC, 251), mean (SD) age ranged from 67 (5) to 76 (6) years across cohorts, with between 55% (137/251) and 74% (95/128) female participants.
Why it matters
In older adults without cognitive impairment, those with elevated amyloid and tau PET signal were much more likely to develop mild cognitive impairment within about 2 to 2.7 years than those in other biomarker groups. This suggests these PET scans may help identify people at near-term risk, which could aid prevention trials, but it does not show any treatment works.
-
66/100
At baseline, there were 436 asymptomatic individuals, 69 patients with prodromal AD, and 127 with AD dementia.
Why it matters
In 632 adults with Down syndrome followed over time, the study tracked clinical and cognitive decline along the Alzheimer disease continuum. The authors say the results support screening from the fourth decade and can inform future prevention trials, but no treatment is tested.
-
Addressing the need for rigorous longitudinal data for the effectiveness of music therapy in people with and at risk for developing AD, this trial aims to enhance knowledge regarding cost-effective interventions with potentially high clinical applicability.
Why it matters
This paper reports the protocol for an ongoing trial comparing music therapy, physical activity, and no intervention on brain plasticity, mood, and cognition in people with or at risk for Alzheimer's disease. No results are available yet, so it cannot say whether these approaches treat, cure, or prevent the disease.
-
Characterization of the genetic landscape of Alzheimer's disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes.
Why it matters
This large genetic study found 75 risk loci for Alzheimer's disease and related dementias and built a genetic risk score linked to future risk or progression from mild cognitive impairment. It identifies genetic risk factors only and reports no treatment, cure or prevention.
-
This cluster randomized clinical trial found that despite high adherence to the training, a multicomponent intervention promoting goal-directed care for suspected UTIs and LRIs did not significantly reduce antimicrobial use among nursing home residents with advanced dementia.
Why it matters
This trial found that a multicomponent intervention promoting goal-directed care did not significantly reduce antimicrobial use among nursing home residents with advanced dementia. It is about infection management in dementia care, not about treating, curing or preventing Alzheimer disease.
-
This fifteen-year study provides a large database of highly characterized individuals with longitudinal cognitive, imaging and lifestyle data and biofluid collections, to aid in the development of interventions to delay onset, prevent or treat AD.
Why it matters
The Australian AIBL study has followed 2,359 people since 2006: 1,112 in the original cohort (cognitively normal, mild cognitive impairment and Alzheimer's dementia) plus 1,247 added later. Each person is retested every 18 months with cognitive tests, MRI and amyloid/tau PET scans, blood biomarkers and lifestyle measures, for more than 8,500 person-years in total. The authors say this has helped define the preclinical, prodromal and clinical stages of Alzheimer's and has made it possible to study factors linked to age at onset and speed of progression. It is a description of a research resource, not a test of any treatment.
-
Increasing evidence indicates that physical activity and exercise training may delay or prevent the onset of Alzheimer's disease (AD).
Why it matters
In 23 asymptomatic late middle-aged adults at risk for Alzheimer's disease, 26 weeks of aerobic exercise training increased plasma Cathepsin B, and changes in Cathepsin B correlated with cognitive performance. BDNF levels decreased with training, and klotho levels were unchanged but closely associated with change in VO2 peak.
-
The ε4 allele of apolipoprotein E (APOE) gene and increasing age are two of the most important known risk factors for developing Alzheimer disease (AD).
Why it matters
This study used cerebrospinal fluid biomarkers to examine how the APOE ε4 risk gene relates to Alzheimer's disease across different ages. It does not test any treatment or prevention, but may help researchers better identify who has Alzheimer's disease for future studies.
-
66/100
We found that amyloid-β-positive cognitively unimpaired individuals were mainly characterized by decreased functional connectivity between the medial temporal lobe and regions in the anterior-temporal system, most prominently between left perirhinal/entorhinal cortices and medial prefrontal cortex.
Why it matters
In people with amyloid in the brain but no cognitive symptoms, decreased connectivity between medial temporal lobe regions was associated with worse memory and faster memory decline. This suggests early brain network changes may precede symptoms, but it does not show how to prevent or treat Alzheimer's disease.
-
66/100
Statistically significant effects of AZD0530 treatment were not found on relative CMRgl reduction in an Alzheimer disease-associated region of interest or on secondary clinical or biomarker measures.
Why it matters
In this trial, AZD0530 did not show statistically significant effects on brain metabolism or on secondary clinical or biomarker measures in people with Alzheimer disease. This means the drug was not shown to be effective in this study.
-
Observational epidemiological studies provide valuable information regarding naturally occurring protective factors observed in populations with very low prevalences of vascular disease.
-
Our analysis extends recent work by revealing specific benefits for instrumental activities of daily living for individuals in the early stages of AD and supports the value of exercise for individuals with cognitive impairment.
Why it matters
In this secondary analysis of a 26-week trial, people with early-stage Alzheimer's disease who did aerobic exercise kept their ability to perform daily activities better than those who did stretching and toning. This suggests exercise may help maintain independence, but it does not show a cure or prevention.
-
Alzheimer's disease (AD) is a progressive neurodegenerative condition marked by a decline in cognitive functions with no validated disease modifying treatment.
Why it matters
This study used a deep learning model combining imaging, spinal fluid, and cognitive data to predict which people with MCI would convert to Alzheimer's disease, reaching 81% accuracy. It is a prediction tool for identifying people for trials, not a treatment, cure, or prevention.
-
This study showed that a simple blood test measuring neurofilament light (NfL), a protein released when brain cells are damaged, can detect the earliest signs of brain degeneration in people carrying genes that cause early-onset familial Alzheimer's disease - years before any symptoms appear.
Why it matters
In people with inherited Alzheimer's disease, the rate of change of serum neurofilament light distinguished mutation carriers from non-carriers about a decade earlier than single measurements and predicted brain shrinkage and cognitive change. This is a marker of progression, not a treatment or cure.
-
The maximal tolerated dose of PQ912 has been identified and the results support future studies at still lower doses reaching > 50% target occupancy, a longer up-titration phase to potentially induce adaptation and longer treatment periods to confirm the early signals of efficacy as seen in this study.
Why it matters
In a phase 2a trial in people with Alzheimer's, the glutaminyl cyclase inhibitor PQ912 cut the target enzyme's activity, reaching an average target occupancy of > 90%, and was linked to a reduction in EEG theta power and better scores on one memory test. Serious adverse events were slightly more common than on placebo, though not significantly different. The authors see only early signals of efficacy and call for longer studies at lower doses.
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.
- Caspase-1 inhibition improves cognition without significantly altering amyloid and inflammation in aged Alzheimer disease mice
- The rate of the Down syndrome among offspring of women with Alzheimer disease
- Deep Brain Stimulation Targeting the Fornix for Mild Alzheimer Dementia (the ADvance Trial): A Two Year Follow-up Including Results of Delayed Activation
- Alzheimer's disease comorbidity in normal pressure hydrocephalus: prevalence and shunt response
- Classification and staging of Parkinson's disease using video-based eye tracking
- Quantification of white matter cellularity and damage in preclinical and early symptomatic Alzheimer's disease
- Diagnostic value of fluid‐based non‐amyloid biomarkers for Alzheimer's disease and related dementias in a clinic‐based cohort from South Asia
- The pattern of atrophy in familial Alzheimer disease: volumetric MRI results from the DIAN study
- Causes and consequences of disturbances of cerebral glucose metabolism in sporadic Alzheimer disease: therapeutic implications
- Neuroinflammation and Alzheimer disease: clinical and therapeutic implications