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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Donanemab and Lecanemab showed good efficacy in ADCS-ADL and CDR-SB, respectively.
Why it matters
This network meta-analysis compared several newer Alzheimer's drugs across cognitive and daily-function scales. It found lecanemab more effective on one scale, donanemab on another, and GV-971 ranked well on two measures, but the authors note controversy remains over how to choose among these drugs.
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Recent expansion of proteomic coverage opens unparalleled avenues to unveil new biomarkers of Alzheimer's disease (AD).
Why it matters
This study analyzed cerebrospinal fluid proteins and found that YWHAG and multi-protein panels diagnosed Alzheimer's disease with high accuracy, validated in an independent cohort and against autopsy-confirmed cases. It is a biomarker study for diagnosis and prediction, not a treatment or cure.
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APP gene dosage is strongly associated with Alzheimer's disease (AD) pathogenesis.
Why it matters
In human stem cell-derived neurons, antisense oligonucleotides targeting APP reduced APP protein levels, rescued endolysosome and autophagy dysfunction, and reduced amyloid-beta aggregates. These are laboratory cell results, and the approach is proposed only for forms of Alzheimer's caused by duplication of the APP gene, including Down syndrome-related Alzheimer's.
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52/100
Importantly, Aβ42/Aβ40 ratio remained unaltered, suggesting that it is more suitable for implementation in clinical workup than individual Aβ peptides.
Why it matters
CSF and plasma amyloid-beta42 and amyloid-beta40 levels fluctuated with time of day, while p-tau, GFAP and NfL did not, and the amyloid-beta42/40 ratio remained stable. This suggests the ratio is more suitable for clinical use than individual amyloid-beta measures, but it does not test any treatment.
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52/100
Defective mitophagy is consistently found in postmortem brain and iPSC-derived neurons from Alzheimer disease (AD) patients.
Why it matters
In 246 people across the Alzheimer's continuum, blood and CSF markers of mitophagy were altered in those with Alzheimer's disease compared with cognitively unimpaired individuals, and the changes correlated with worse clinical measures. This shows mitophagy impairment can be reflected in biofluid markers, but it does not test any treatment, cure or prevention.
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Since the development of amyloid tracers for PET imaging, there has been interest in quantifying amyloid burden in the brains of patients with Alzheimer disease.
Why it matters
This report summarizes an expert workshop on measuring amyloid burden with PET imaging for staging and monitoring Alzheimer's disease. It notes that significant challenges remain before quantitative amyloid PET can be used widely in clinical practice, and it does not address treatment, cure, or prevention.
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The ɛ4 allele of the apolipoprotein E gene (APOE), which translates to the APOE4 isoform, is the strongest genetic risk factor for late-onset Alzheimer disease (AD).
Why it matters
This review describes how the APOE4 risk gene acts differently in different brain cell types, with APOE4 in neurons proposed as an early driver of the disease process. It is a summary of research and a proposed model, not a treatment or cure, though it points to possible future therapeutic directions.
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Alzheimer's disease (AD) is the leading cause of dementia, presenting a significant unmet medical need worldwide.
Why it matters
This update reviews Alzheimer drug trials from 2020 to 2023 and notes that the FDA approved aducanumab and lecanemab, both amyloid-targeting antibodies, ending nearly two decades without new Alzheimer drugs. It is a report on the trial landscape, not evidence that these drugs cure or prevent the disease.
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Candidate cis-regulatory elements (cCREs) in microglia demonstrate the most substantial enrichment for Alzheimer's disease (AD) heritability compared to other brain cell types.
Why it matters
By combining genetic data with microglia-specific 3D genome maps, researchers identified 308 previously unreported Alzheimer's risk variants at 181 regulatory elements and linked some to target genes. This expands understanding of how genetic risk acts through microglia, but it is a genetic mapping study, not a treatment or prevention trial.
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Proteomic studies for Alzheimer's disease (AD) are instrumental in identifying AD pathways but often focus on single tissues and sporadic AD cases.
Why it matters
This proteomic study measured proteins in brain, cerebrospinal fluid, and plasma and found signatures that distinguished sporadic Alzheimer's disease and TREM2 variant carriers from controls. It is about molecular signatures and diagnosis, not about treating, curing, or preventing the disease.
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Although pathogenic variants in PSEN1 leading to autosomal-dominant Alzheimer disease (ADAD) are highly penetrant, substantial interindividual variability in the rates of cognitive decline and biomarker change are observed in ADAD.
Why it matters
Among carriers of inherited PSEN1 variants in the DIAN study, those whose variant affects the transmembrane part of the protein had worse thinking, smaller hippocampus and higher phosphorylated tau than carriers of cytoplasmic variants, despite similar amyloid levels. The authors say variant location may explain much of the person-to-person difference in disease course, which matters for designing and interpreting clinical trials in inherited Alzheimer's.
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52/100
Our results highlight the efficacy of founder populations for AD genetic studies.
Why it matters
In people of Ashkenazi Jewish ancestry, this study confirmed known Alzheimer's genes like APOE and TREM2 and found additional associations near RAB3B, SPOCK3, ANXA10, SMAP2, and GIPR. These results show that studying founder populations can help uncover genetic risk factors for Alzheimer's disease.
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Previous studies reported the value of blood-based biomarkers in predicting Alzheimer disease (AD) progression among individuals with different disease stages.
Why it matters
In 251 people with amnestic mild cognitive impairment followed up to 8 years, baseline blood Aβ42/Aβ40 and p-tau181 predicted long-term clinical progression to Alzheimer's disease. This is a prediction study, so it does not show that any treatment, cure or prevention works.
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Imaging of amyloid deposition using PET has been available in research studies for 2 decades and has been approved for clinical use by the U.S. Food and Drug Administration, the European Medicines Agency, and other regulatory agencies around the world.
Why it matters
This review describes amyloid PET as a tool for diagnosing Alzheimer's disease by detecting amyloid plaques, and notes its expected increased use with the approval of the antiamyloid antibody aducanumab. It covers diagnosis and a treatment approval, but does not report that amyloid PET itself treats, cures, or prevents Alzheimer's disease.
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52/100
This was then correlated with overall cortical flortaucipir PET and PiB PET standardized uptake value ratio (SUVr).
Why it matters
In dementia with Lewy bodies patients, reduced posterior default mode network connectivity correlated with higher cortical tau and amyloid PET uptake. This describes how Alzheimer co-pathology relates to brain network changes and does not report a treatment, cure or prevention.
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Conventional MCI criteria were insufficient to allow for the creation of well-defined and internationally comparable samples of MCI patients.
Why it matters
This analysis compared five mild cognitive impairment datasets and found that despite similar baseline characteristics, the samples differed markedly in subsequent cognitive performance and clinical development. The goal is to create a standard control algorithm to help reduce the number of participants exposed to placebo in future prevention trials.
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AD is a neurodegenerative disease, and its frequency is often reported to be higher for women than men: almost two-thirds of patients with AD are women.
Why it matters
This review discusses why Alzheimer's disease is more common in women, noting that women live longer and that differences in risk at the same age are hard to assess with mixed findings. It does not report a treatment, cure or prevention.
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Although synovitis is the pathological hallmark of rheumatoid arthritis (RA), many extra-articular manifestations (EMs) and comorbidities likely occur due to the complex, chronic, inflammatory, and autoimmune features of RA.
Why it matters
This overview notes evidence that microvascular cerebral damage caused by systemic inflammation is associated with the development of Alzheimer's disease and vascular dementia. It also mentions that some observational studies have hinted how Disease Modified Anti-Rheumatic Drugs and biologics could reduce the incidence of dementia.
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52/100
Defining a signature of cortical regions of interest preferentially affected by Alzheimer disease (AD) pathology may offer improved sensitivity to early AD compared to hippocampal volume or mesial temporal lobe alone.
Why it matters
Cortical signature maps on MRI were sensitive to early amyloid increases in asymptomatic individuals within their own cohorts but performed poorly across late-onset and autosomal dominant Alzheimer disease cohorts. This suggests the pattern of early brain change differs between these forms of the disease, but it is an imaging finding and not a treatment.
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Our results provide evidence of frontal cortical involvement of tau pathology in behavioral/dysexecutive AD and highlight the need for consensus clinical criteria in this syndrome.
Why it matters
In patients with biologically defined behavioral/dysexecutive Alzheimer disease, frontal cortical tau aggregation was found with peaks in medial prefrontal, anterior cingulate, and frontal insular cortices, in contrast to amnestic Alzheimer disease, while no differences were observed in amyloid-PET distribution or atrophy. Tau-PET uptake in these regions best differentiated behavioral/dysexecutive from amnestic Alzheimer disease, but this is a small study of 15 patients and reports no treatment, cure, or prevention.
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Alzheimer's disease (AD) is currently untreatable, and therapeutic strategies aimed to slow cognitive decline have not yet been successful.
Why it matters
This review argues that because genome-wide association studies have identified Alzheimer's disease risk factors in genes expressed in microglia, these microglial functions could be targeted therapeutically to modulate microglial cell state and slow disease progression. It describes potential approaches rather than reporting a proven treatment, cure or prevention.
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The aim of this study is to use classification methods to predict future onset of Alzheimer's disease in cognitively normal subjects through automated linguistic analysis.
Why it matters
This study used automated linguistic analysis of written responses to predict future onset of Alzheimer's disease in cognitively normal participants. It is a predictive modeling study of a possible early marker and does not test any treatment, cure, or prevention.
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Cerebrospinal fluid analyses and neuroimaging can identify the underlying pathophysiology at the earliest stage of some neurodegenerative disorders, but do not have the scalability needed for population screening.
Why it matters
This review describes how blood-based markers for neurodegenerative disorders other than Alzheimer disease are still at an early stage, with research so far focused mainly on Alzheimer disease. It does not report any treatment, cure or prevention, only the potential usefulness of such markers for screening and diagnosis.
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52/100
Polygenic risk scores have identified that genetic variants without genome-wide significance still add to the genetic risk of developing Alzheimer's disease (AD).
Why it matters
In mice with amyloid-β pathology, but not in mice with tau pathology, a group of genes rich in Alzheimer risk genes switched on in microglia, the brain's immune cells. The group included 7 well-known risk genes such as APOE, CD33 and PLCG2, plus 11 genes that genetic studies had flagged only weakly. The authors conclude that genetic risk acts through the microglial response to amyloid, before tau, but this is gene-activity data from two mouse models, not a test of any treatment or of risk in people.
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Alzheimer disease (AD) accounts for 60-70% of dementia cases.
Why it matters
This review states that currently available Alzheimer's drugs, cholinesterase inhibitors and an NMDA receptor antagonist, can only inhibit symptoms for a limited time and cannot stop or reverse disease progression. It reports no new treatment, cure or prevention.
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.
- Cerebral Amyloid Angiopathy and Risk of Dementia in Patients With Cognitive Complaint
- Effects of Experimental Periodontitis and Periodontal Treatment on Alzheimer‐Like Pathology in Rats
- Production and increased detection of amyloid beta protein and amyloidogenic fragments in brain microvessels, meningeal vessels and choroid plexus in Alzheimer's disease
- Progression-Aware and Explainable CNN–Transformer Framework for Multiclass Alzheimer’s Disease Staging Using MRI
- Longitudinal Cerebrospinal Fluid Biomarker Changes in Preclinical Alzheimer Disease During Middle Age
- Association of Plasma Biomarkers of Alzheimer Disease and Neurodegeneration With Longitudinal Intra-Network Functional Brain Connectivity
- Advantages and disadvantages of the use of the CSF Amyloid β (Aβ) 42/40 ratio in the diagnosis of Alzheimer's Disease
- Alcohol consumption and cerebrospinal fluid biomarkers for preclinical alzheimer's disease in a population-based sample of 70-year-olds
- Evaluation of the Revised Criteria for Biological and Clinical Staging of Alzheimer Disease
- Adult-onset deactivation of autophagy leads to loss of synapse homeostasis and cognitive impairment, with implications for alzheimer disease