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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Higher AD-PRS was associated with faster CD in the full clinical cohort and in biomarker subset, independently of APOE genotype.
Why it matters
A higher Alzheimer polygenic risk score was linked to faster cognitive decline over time, independent of APOE genotype, but it did not predict baseline cognitive test scores. The added predictive value beyond routinely available clinical variables was modest, and model performance was not consistently reproducible across cohorts.
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BackgroundAmyloid-negative tau-related neurodegeneration represents a non-Alzheimer biomarker-defined profile; however, its clinical heterogeneity and prognostic relevance remain unclear within Alzheimer's disease-related frameworks.
Why it matters
Among 130 patients with an amyloid-negative but tau-elevated cerebrospinal fluid pattern, this retrospective cohort found heterogeneous diagnoses and that survival differed across diagnostic groups, with higher cerebrospinal fluid total tau predicting mortality. It describes prognosis in a non-Alzheimer biomarker profile and does not offer treatment, cure, or prevention.
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Of the 500 eligible participants (71% female, 95% non-Latino White, mean [SD] age at cohort dementia onset = 88 [7] years, mean [SD] years from onset to death = 4 [3]), only 54% received a timely diagnosis.
Why it matters
In this cohort of 500 deceased older adults, only 54% received a timely dementia diagnosis, and those with a pathologic diagnosis of AD or moderate/severe LATE-NC were more likely to be diagnosed in a timely manner. This suggests the healthcare system more readily captures certain neuropathologies, but the findings need replication in broader populations.
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Between 2000 and 2024, deaths from stroke, heart disease, and HIV decreased, whereas reported deaths from AD increased 134%.
Why it matters
This report estimates that 7.4 million Americans age 65 and older live with clinical Alzheimer's dementia today, a number that could reach 13.8 million by 2060 absent medical breakthroughs that prevent or cure the disease. It describes the public health burden, including 116,022 recorded deaths in 2024 and the costs of unpaid caregiving, rather than testing any treatment.
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The Centiloid method demonstrates strong intertracer and interscanner harmonization when standardized to the 11C-Pittsburgh compound B reference, with high correlation (r2 > 0.9) across 18F-labeled tracers, including florbetapir, flutemetamol, and florbetaben.
Why it matters
This review reports that the Centiloid scale harmonizes amyloid PET measurements across tracers and scanners, with most articles identifying a threshold of 20 to 25 Centiloids as indicating significant amyloid pathology. It is a standardization tool for research and clinical decision-making, not a treatment or cure.
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Appetite disturbances were present in 9.4% of participants and were associated with greater neuropsychiatric burden and disease severity.
Why it matters
This study found that appetite disturbances were present in 9.4% of participants and were linked to greater disease severity, with lower gray matter volume showing the strongest association. It describes a possible early behavioral marker and does not test any treatment, cure, or prevention.
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Novel insights into Alzheimer's disease through the study of individuals with Down syndromePeople with Down syndrome (DS) represent the largest genetically defined population at risk for Alzheimer's disease (AD). 1 Virtually all adults with DS develop AD neuropathology by midlife due to triplication of the amyloid precursor protein (APP) gene on chromosome 21.As medical advances and social integration have extended life expectancy into the 60s, AD has emerged as the major determinant of cognitive decline, morbidity, and mortality in this DS population. 2 What was once viewed as an inevitable consequence of aging in DS is now recognized as a unique scientific opportunity to uncover the earliest events that drive AD.The predictable and accelerated course of DS-associated AD (DSAD) provides an unparalleled window into the molecular and cellular origins of amyloid and tau pathology, neuroinflammation, cerebrovascular pathology, and neurodegeneration.
Why it matters
This review explains that studying people with Down syndrome, who almost all develop Alzheimer's pathology by midlife, offers a unique chance to understand the earliest steps of the disease. This knowledge could help prevent Alzheimer's not only in Down syndrome but also in the broader population.
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47/100
Our study included 74,275 weeks of driving data (2015-2024, average follow-up 6.1 years).
Why it matters
This study found that more white matter hyperintensities were linked to simpler driving patterns over time, and that in people developing cognitive impairment, risky driving events increased. It suggests these brain changes may help identify people at risk of unsafe driving, but it does not test a treatment, cure, or prevention.
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SSRI treatment showed no significant effect on AD dementia progression (hazard ratio = 1.64, 95% confidence interval: 0.61 to 4.38) or cognitive trajectories, regardless of AD pathology.
Why it matters
This study found that SSRI treatment had no significant effect on progression to Alzheimer's disease dementia or cognitive trajectories in people with amnestic mild cognitive impairment, regardless of Alzheimer's pathology. SSRIs also did not affect amyloid accumulation or cortical thickness.
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This review covers recent advances (2023-2024) in neuroimaging research into the pathophysiology, progression, and treatment of Alzheimer's disease (AD) and related dementias (ADRD).
Why it matters
This review describes how brain imaging is used to visualize and track amyloid, tau, neurodegeneration, inflammation and vascular disease in Alzheimer's and related dementias. It reports technical and biomarker advances, not a treatment or cure, and notes that tau PET harmonization remains challenging.
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BackgroundAs the prevalence of Alzheimer disease (AD) rises, early identification of at-risk individuals is essential for effective intervention.
Why it matters
This study looked at whether mild behavioral impairment is linked to Alzheimer's biomarkers in spinal fluid in people without dementia. It is early observational work and does not show that treating these symptoms changes disease course.
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In the LA cohort only, higher WMHs load was associated with greater GM atrophy across all groups (HCs, AD, bvFTD), with a specific neurodegenerative pattern involving orbitofrontal, cingulate, and temporal areas.
Why it matters
In the Latin American cohort, higher white matter hyperintensities load was associated with greater gray matter atrophy across all groups, and healthy controls from Latin America showed a greater white matter hyperintensities load than their US counterparts. The study is about geographic variations in white matter hyperintensities and their impact on brain structure and function, not about treating, curing, or preventing Alzheimer's disease.
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ε4, socioeconomic status, physical activity, smoking, subjective cognitive decline, and various cardiovascular risk factors and comorbidities.
Why it matters
In this African American cohort, a higher proportion of genetically inferred African ancestry was suggestively linked to a slower rise in blood p-Tau181 over time, and genetic factors tied to Alzheimer's in European cohorts were not linked to the three biomarkers studied. The authors state more research is needed, so this offers no treatment, cure or prevention.
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47/100
This study provided a preliminary examination of indices of obstructive sleep apsnea (OSA) and sleep disruptions in adults with Down syndrome (DS), and their associations with Alzheimer's disease (AD) pathology and symptomatology.
Why it matters
In this preliminary study of 93 adults with Down syndrome, most screened positive for obstructive sleep apnea, many without a prior diagnosis, and greater wake percentage and shorter sleep time were associated with higher amyloid and tau burden. The authors describe this as preliminary evidence linking sleep disruption and sleep apnea with Alzheimer's-related pathology, and no treatment for Alzheimer's disease is tested.
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The early and accurate diagnosis of Alzheimer's Disease and Frontotemporal Dementia remains a critical challenge, particularly with traditional machine learning models which often fail to provide transparency in their predictions, reducing user confidence and treatment effectiveness.
Why it matters
A deep learning framework classified Alzheimer's disease, frontotemporal dementia, and healthy controls from EEG data with accuracies of 99.7% for binary tasks and 80.34% for multi-class classification. This is a diagnostic classification method and does not treat, cure, or prevent Alzheimer's disease.
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Alzheimer's disease (AD) represents the most prevalent neurodegenerative disorder and leading cause of dementia worldwide, with its incidence rising dramatically in aging populations.
Why it matters
This review states that current therapies, including recently approved anti-amyloid immunotherapies, have limited clinical efficacy and significant adverse effects, and that no truly disease-modifying therapy exists. It surveys possible future strategies such as tau-targeting and anti-inflammatory agents but does not report a proven treatment or cure.
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47/100
Alzheimer's disease (AD) is a progressive neurodegenerative disorder that significantly impacts cognitive function, posing a major global health challenge.
Why it matters
This study presents a deep learning framework using MRI and PET data for early detection of Alzheimer's disease and reports 99.87% accuracy with a Softmax classifier. It is a technical diagnostic study and does not test any treatment, cure, or prevention.
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This study aims to assess the evolution of cognitive performances over a 5-year follow-up period in community-dwelling older people with negative plasma p-tau181 levels and to determine whether frailty could discriminate between those who experience cognitive decline and those who do not, in the p-tau negative groups.
Why it matters
This 5-year analysis of the MAPT trial assessed cognitive change in community-dwelling older people with negative plasma p-tau181 and whether frailty distinguished those who declined. It describes the course of people without the biomarker and does not test a treatment, cure or prevention.
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Of 1309 new patients, 514 (39% of new patients) had clinical mild cognitive impairment (MCI) or AD.
Why it matters
In a tertiary memory clinic, only 8 percent of all new patients and 21 percent of those with clinical mild cognitive impairment or Alzheimer disease initially met criteria for anti-amyloid treatment. After further exclusions such as apolipoprotein E ε4/ε4 homozygosity and anticoagulant use, eligibility fell to 6 percent of all patients and 15 percent of those with clinical MCI or AD.
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Alzheimer's disease (AD) is increasingly recognized as a disorder not solely of amyloid and tau accumulation but also of chronic immune dysregulation.
Why it matters
This review argues that neuroinflammation, including sustained microglia and astrocyte activation and inflammasome activation, contributes to Alzheimer's disease progression, and that inflammatory genes and immune pathways are linked to disease risk. It discusses the rationale for anti-inflammatory treatments but does not report a tested treatment or cure.
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The relation between vitamin A (VA) level and cognitive function and the underlying mechanisms have not been thoroughly investigated.
Why it matters
This study combined a population analysis of 1,817 adults aged 50 and above with an animal experiment, finding that higher plasma vitamin A was linked to lower mild cognitive impairment risk and that low vitamin A worsened Alzheimer's-like pathology in mice. The human part is cross-sectional and the animal part is early-stage, so it cannot show that vitamin A treats, cures, or prevents Alzheimer's disease.
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47/100
We show reduced fiber cross-section in LBD versus PD, and increased concentrations of plasma neurofilament light chain and p-tau217; with p-tau217 and fiber cross-section associated with cognition.
Why it matters
The presence of dementia in Lewy body disease was associated with poorer white matter macrostructure and may relate to pathological protein accumulation, with plasma neurofilament light and p-tau217 increased relative to Parkinson's disease and controls. Differences between dementia with Lewy bodies and Parkinson's disease dementia may be driven by other factors distinct from those driving dementia.
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47/100
Bibliometric analysis is crucial in identifying research gaps and trends and guiding future studies to address unmet needs in understanding and modeling human physiology and pathology.
Why it matters
This analysis of 531 articles tracks how research using human stem cell-derived brain cells (hiPSC models) to study Alzheimer's has grown since 2010, led by the United States and then China. Recent work has focused on inflammation, astrocytes, microglia, ApoE and tau. It maps research activity rather than testing treatments, but the authors argue these human cell models can build a foundation for future therapies.
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47/100
After adjusting for various factors, the incidence of Alzheimer dementia was significantly higher in the anosmia group compared to the control group (hazard ratio [HR], 1.15; 95% CI, 1.04-1.28).
Why it matters
This cohort study found that a diagnosis of anosmia in middle age was associated with a higher risk of Alzheimer dementia, while no significant increase was observed in those over 65. Vascular dementia was not statistically associated with anosmia.
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47/100
Menopause is a major biological transition that may influence women's late-life brain health.
Why it matters
Among 268 women in an autopsy cohort, earlier menopause strengthened the links between reduced synaptic integrity and faster cognitive decline and higher tau tangles, and these relationships appeared weaker in women who took menopausal hormone therapy. These are observational findings, so they do not show that hormone therapy or any other intervention prevents or treats Alzheimer's disease.
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.
- A randomized placebo-controlled pilot trial of omega-3 fatty acids and alpha lipoic acid in Alzheimer's disease
- Sex differences in amyloid PET in a large, real‐world sample from the Imaging Dementia–Evidence for Amyloid Scanning (IDEAS) Study
- Emotion recognition in Huntington's disease and frontotemporal dementia
- Diet therapy for the treatment of Alzheimer's disease in view of traditional Persian medicine: A review
- Baseline Imaging Characteristics of Participants in the Phase II/III DIAN‐TU‐001 Tau NexGen Trial for Dominantly Inherited Alzheimer’s Disease
- APOE2 eases cognitive decline during Aging: Clinical and preclinical evaluations
- Cerebrospinal Fluid Biomarkers of Alzheimer Disease
- The Role of Oxidative Damage in the Pathogenesis and Progression of Alzheimer's Disease and Vascular Dementia
- High-sensitivity plasma proteomics reveals disease-specific signatures and predictive biomarkers of Alzheimer's disease phenotypes in a large mixed-dementia cohort
- Current status on Alzheimer disease molecular genetics: from past, to present, to future