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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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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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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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.
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Models of Alzheimer's disease (AD) pathophysiology posit that amyloidosis [A] precedes and accelerates tau pathology [T] that leads to neurodegeneration [N].
Why it matters
This study compared the longitudinal trajectories of Alzheimer's ATN biomarker profiles in non-demented elderly adults. It investigated whether biomarker sequences other than the usual amyloid-tau-neurodegeneration order are possible.
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Nationwide population-based cohort provides a new opportunity to build an automated risk prediction model based on individuals' history of health and healthcare beyond existing risk prediction models.
Why it matters
Using Korean national health-insurance records for 40,736 people over 65, this study tested whether machine learning could predict who would later be diagnosed with Alzheimer's from routine health data, reaching an AUC of 0.775 for one-year prediction and lower values (0.644–0.730) at longer horizons. Hemoglobin level, age and urine protein level were among the features the model leaned on, which signals statistical association, not a cause or a target for treatment. The authors frame it as a step toward picking at-risk people for clinical trials or earlier detection; it is not a diagnostic test and does not test any treatment.
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This study reviews recent advances in understanding the complex pathobiology of Alzheimer disease and discusses current treatment strategies.
Why it matters
An update on the disease biology of Alzheimer's disease and on strategies for treating it.
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Symptomatic mutation carriers also demonstrated elevated tau PET binding in the basal ganglia, consistent with prior work with amyloid-β.
Why it matters
In this study of autosomal dominant Alzheimer disease, tau PET binding was elevated in the basal ganglia of symptomatic mutation carriers and was tied to the onset of cognitive dysfunction. It describes a biomarker pattern in an inherited form of the disease, not a treatment, cure, or prevention.
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In contrast to no change in global cortical SUVR in the CU- and CU+ groups during the 2-y period, global cortical SUVR increased by 0.06 (2.9%) in the MCI+ group and 0.19 (8.0%) in the DEM+ group at follow-up.
Why it matters
Over two years, tau accumulation increased in people with mild cognitive impairment and in those with dementia, but not in cognitively normal groups. Progressive tau buildup in certain cortical areas was linked to worsening cognition, supporting tau PET as a way to monitor Alzheimer's progression.
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The quality of included studies with only a few longitudinal studies, limits the conclusions which may be drawn from the present findings especially regarding the biomarkers other than hippocampal volume.
Why it matters
This systematic review of 40 observational studies found that the majority did not show a significant association between physical activity and Alzheimer disease biomarkers. The authors note that few longitudinal studies limit the conclusions, so this does not establish that physical activity changes Alzheimer pathology.
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We hypothesize that CRP (C-reactive protein) is associated with brain structural changes and may interact with amyloid to produce vascular and degenerative damage.
Why it matters
This study examined whether C-reactive protein levels were associated with brain structural changes and interacted with amyloid to produce vascular and degenerative damage. The role of inflammation in cerebral small vessel disease and neurodegeneration remains poorly understood, and this research explored the joint effects of CRP and plasma amyloid-β levels.
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Amyloid deposition and neurofibrillary degeneration in Alzheimer's disease specifically affect discrete neuronal systems, but the underlying mechanisms that render some brain regions more vulnerable to Alzheimer's disease pathology than others remain largely unknown.
Why it matters
This study compared brain imaging patterns of amyloid and neurodegeneration in people with Alzheimer's dementia against healthy controls, and related those patterns to gene expression in different brain regions. It is an analysis of existing human data that may help explain why some brain areas are more vulnerable, but it does not test any treatment, cure, or prevention.
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59/100
A growing body of evidence suggests that the plasma concentration of the neurofilament light chain (NfL) might be considered a plasma biomarker for the screening of neurodegeneration in Alzheimer's disease (AD).
Why it matters
Plasma neurofilament light was measured in 99 subjects with Alzheimer's disease at the mild cognitive impairment or early dementia stage and in non-demented controls. This work is about a possible biomarker for detecting neurodegeneration, not about treating, curing or preventing the disease.
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59/100
Arterial stiffness, measured by PWV, is an emerging risk factor for dementia through its repeated relationships with cognition, cSVD, and Aβ deposition.
Why it matters
In this cross-sectional study, greater central arterial stiffness was associated with greater amyloid-β deposition in the brain and with lower brain volumes in Alzheimer disease-sensitive regions. The study shows an association only and does not show that reducing arterial stiffness treats, cures, or prevents Alzheimer's disease.
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We describe the first large-scale, potentially label-enabling clinical trial of a preclinical treatment for ADAD.
Why it matters
This phase 2 trial is testing whether the antiamyloid antibody crenezumab can prevent or delay symptoms in people who carry a PSEN1 E280A mutation and are destined to develop Alzheimer's disease. The study is designed to measure changes in cognitive test scores and time to progression to mild cognitive impairment or dementia over 260 weeks.
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.
- Associations of blood cell indices and anemia with risk of incident dementia: A prospective cohort study of 313,448 participants
- Roles of vascular and metabolic components in cognitive dysfunction of Alzheimer disease: short- and long-term modification by non-genetic risk factors
- An explainable and efficient deep learning framework for EEG-based diagnosis of Alzheimer's disease and frontotemporal dementia
- 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