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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59/100
Alzheimer's disease (AD) is the leading cause of dementia globally, having a pathophysiology that is complex and multifactorial.
Why it matters
This systematic review gathers evidence on four kinds of non-coding RNAs, molecules that regulate genes without making proteins, in Alzheimer's disease. They are involved in amyloid-beta clumping, tau changes, inflammation and other disease processes, and may serve as markers for early detection and as new treatment targets. The authors stress that more research is needed to confirm their clinical usefulness.
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Higher baseline p-tau181 and NfL were associated with significantly faster decline in most cognitive, physical, and functional outcomes (+1 SD p-tau181: β MMSE = -0.055, 95% CI -0.067 to -0.043, β FCSRT = -0.034, 95% CI -0.043 to -0.025, β fluency = -0.029, 95% CI -0.038 to -0.020, β SPPB = -0.040, 95% CI -0.057 to -0.022, and β 4IADL = -0.115, 95% CI 0.091-0.140. +1 SD NfL: β MMSE = -0.039, 95% CI -0.053 to -0.025, β FCSRT = -0.022, 95% CI -0.032 to -0.012, β fluency = -0.014, 95% CI -0.024 to -0.004, and β 4IADL = 0.077, 95% CI 0.048-0.105).
Why it matters
In this cohort, higher baseline p-tau181 and NfL were linked to faster decline in several cognitive, physical, and functional measures. The study only describes how these blood markers relate to later decline; it does not test any treatment or prevention.
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Alzheimer disease (AD) is primarily associated with accumulations of amyloid plaques and tau tangles in gray matter, however, it is now acknowledged that neuroinflammation, particularly in white matter (WM), significantly contributes to the development and progression of AD.
Why it matters
In 310 older participants, this cross-sectional study used a diffusion imaging measure to look at white matter neuroinflammation across the Alzheimer's continuum and its links to pathology and cognition. It explores a possible contributor to disease but does not test any treatment or prevention.
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Unlike previous research that used traditional immunoassay, recent studies that measured plasma Aβ42/40 using fully automated platforms reported promising results.
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We characterized the world's second case with ascertained extreme resilience to autosomal dominant Alzheimer's disease (ADAD).
Why it matters
This case report describes a man with an inherited Alzheimer-causing mutation who remained cognitively intact until age 67 and carried a rare RELN variant called COLBOS. The finding suggests a role for RELN signaling in resilience to dementia, but it comes from a single case and mouse work, so it is very early.
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An estimated 40% of dementia is potentially preventable by modifying 12 risk factors throughout the life course.
Why it matters
This genetic analysis aimed to identify which modifiable risk factors are causally linked to Alzheimer's disease to guide prevention and drug targeting. It is an analysis of genetic associations and does not report a treatment, cure, or proven prevention.
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Slow paced breathing via heart rate variability (HRV) biofeedback stimulates vagus-nerve pathways that counter noradrenergic stress and arousal pathways that can influence production and clearance of Alzheimer's disease (AD)-related proteins.
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Our ancestry-aware regression approach showed that AA individuals have a lower risk of AD if they inherited African ancestry admixture block at the 17p13.2 locus.
Why it matters
This study identified two genetic regions on chromosomes 17 and 18 linked to Alzheimer's disease in African American individuals, and found that inheriting African ancestry at the 17p13.2 region was associated with lower risk. These findings highlight genes like MINK1, KIF1C, and BCL2 that may matter for Alzheimer's risk in this population.
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The positive association of choline for cognition has been reported in both animal and human studies, yet the associations of choline with the risks of incident dementia or Alzheimer's disease (AD) in humans is unclear.
Why it matters
This study tested whether lower or higher dietary choline intake is associated with increased or decreased risks of incident dementia and Alzheimer's disease using Framingham Heart Study Offspring Cohort data. It is observational, so it cannot show that changing choline intake would prevent dementia or Alzheimer's disease.
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In this retrospective study, GAP-43 was measured in participants from the AD Neuroimaging Initiative (ADNI) cohort using an in-house ELISA method, and levels were compared between groups, both cross-sectionally and longitudinally.
Why it matters
This retrospective study measured cerebrospinal fluid GAP-43 and tested its associations with Alzheimer's disease biomarkers, cognitive decline, and progression to dementia in amyloid-positive individuals. It is about a possible marker of decline, not about treating, curing, or preventing Alzheimer's disease.
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Longitudinal OEF change in older adults is primarily related to vascular pathology.
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Our results indicate good diagnostic and prognostic performance of the plasma p-tau217+ Janssen assay, similar to the p-tau217 Lilly assay.
Why it matters
This study found that a new plasma p-tau217 assay performed similarly to an established assay in detecting amyloid-β status, distinguishing mild cognitive impairment from controls, and predicting conversion to Alzheimer's dementia. It is a diagnostic and prognostic biomarker study and does not test any treatment, cure or prevention.
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Our findings support an association of APOE ɛ4 and p-tau181 with preclinical AD and hippocampus functioning.
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Adults with Down syndrome develop the neuropathological hallmarks of Alzheimer's disease and are at very high risk of developing early-onset dementia, which is now the leading cause of death in this population.
Why it matters
Adults with Down syndrome develop the brain changes of Alzheimer's disease and are at very high risk of early-onset dementia, but there are currently no treatments to prevent it. The review argues that this group could be an optimal population for Alzheimer's prevention trials, though no such preventive treatment yet exists.
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A biological research framework to define Alzheimer' disease with dichotomized biomarker measurement was proposed by National Institute on Aging-Alzheimer's Association (NIA-AA).
Why it matters
This longitudinal study used tau PET to stage how tau spreads in the brain and found that cognitive decline began early, when tau had only increased in transentorhinal regions. The authors state that further validation in other cohorts is needed, so this is a research framework rather than a treatment or cure.
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These findings highlight the diagnostic and longitudinal monitoring potential of GFAP and p-tau for preclinical AD.
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PET, CSF and plasma biomarkers of tau pathology may be differentially associated with Alzheimer's disease (AD)-related demographic, cognitive, genetic and neuroimaging markers.
Why it matters
This study found that tau-PET, CSF, and plasma biomarkers of tau pathology convey partly independent information about Alzheimer's disease. The findings are about comparing biomarkers and do not report on treating, curing, or preventing Alzheimer's disease.
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CSF Aβ 42 and PiB PET showed maximal correlation when collected within 6 years of each other ( R ≈ -0.5).
Why it matters
In 371 participants, CSF and neuroimaging measures of amyloid, tau, and neurodegeneration correlated best within specific time windows, such as CSF Aβ42 and PiB PET within 6 years. This is a biomarker timing study and does not test any treatment, cure, or prevention for Alzheimer's disease.
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Alzheimer's disease (AD) is the most prevalent form of dementia and is characterized by abnormal extracellular aggregates of amyloid-β and intraneuronal hyperphosphorylated tau tangles and neuropil threads.
Why it matters
Brain immune cells called microglia are implicated in Alzheimer's, but how they respond as amyloid plaques and then tau tangles build up in the human brain had been unknown; a reactive form had been described mainly in mice. By reading gene activity in 482,472 individual cell nuclei from brains of people without dementia and from Alzheimer's brains with amyloid only or with amyloid plus tau, this study reports distinct microglia profiles associated with amyloid-β and with tau. It is an observational study of post-mortem tissue: it shows association, not cause, and tests no treatment.
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Reduced hippocampal volume is a biomarker for neurodegeneration, but atrophy is not an AD-specific measure.
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These optimized thresholds can help to inform future research and clinical trials targeting early Aβ.
Why it matters
In three independent samples of clinically normal individuals, the lowest amyloid-PET thresholds that predicted future amyloid accumulation and cognitive decline converged within a short range. This is about defining an imaging threshold for early research and trials, not about treating, curing or preventing Alzheimer disease.
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CVR was significantly associated with cognitive performance independently of AD pathology.
Why it matters
In this cross-sectional study of 72 older people, lower whole-brain cerebrovascular reactivity was linked to worse cognitive performance even after accounting for Alzheimer's biomarkers in spinal fluid. This is an association at a single point in time and does not show that improving blood vessel function would prevent or treat dementia.
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Our work shows that peripheral differential methylation between age-matched subjects with AD relative to healthy controls will provide opportunities to further investigate and validate differential methylation as a surrogate of disease.
Why it matters
This study found differences in DNA methylation in blood between people with Alzheimer's disease, mild cognitive impairment, and healthy controls, and the most significant methylation sites also tracked with cognitive test scores. These findings are preliminary and need further study before blood methylation could be used as an early diagnostic marker.
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Between Feb 1, 2013, and June 28, 2019 (Barcelona), and between June 1, 2009, and Dec 31, 2014 (Cambridge), we included 388 participants with Down syndrome (257 [66%] asymptomatic, 48 [12%] with prodromal Alzheimer's disease, and 83 [21%] with Alzheimer's disease dementia) and 242 euploid controls.
Why it matters
Studied 388 adults with Down syndrome in Barcelona and Cambridge, plus 242 controls, to map when Alzheimer's biomarkers change. Some spinal fluid and blood markers changed as early as the third decade of life, with hippocampal atrophy and changes in cognition in the fifth decade, and prodromal Alzheimer's was diagnosed at a median age of 50.2 years and dementia at 53.7 years.
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Nilotinib is safe and achieves pharmacologically relevant cerebrospinal fluid concentrations.
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.
- Integrated algorithm combining plasma biomarkers and cognitive assessments accurately predicts brain β-amyloid pathology
- Alterations of human CSF and serum-based mitophagy biomarkers in the continuum of Alzheimer disease
- Relationship between beta amyloid peptide generating molecules and neprilysin in Alzheimer disease and normal brain
- A head-to-head comparison of plasma biomarkers to detect biologically defined Alzheimer in a memory clinic
- Genetics of Alzheimer's disease
- Global burden, spatiotemporal disparities, and sex-specific trends of early- and late-onset Alzheimer’s disease and other dementias: a comparative analysis and projections to 2035
- Association of hypometabolism and amyloid levels in aging, normal subjects
- Distinguishing Alzheimer's disease from other major forms of dementia
- Serum triglycerides in Alzheimer disease: Relation to neuroimaging and CSF biomarkers
- Postmortem MRI and histology demonstrate differential iron accumulation and cortical myelin organization in early- and late-onset Alzheimer's disease