Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.
Highest usefulness score first. Studies without a score come last.
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EOAD, although sharing genes with LOAD, harbors unique genes and pathways that could be used to create better prediction models or target identification.
Why it matters
This genetic study found eight new gene regions linked to early-onset Alzheimer's disease, involving microglia activation, glutamate production, and signaling pathways. These findings could help build better prediction models or identify new treatment targets, though they are genetic associations rather than proven treatments.
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Our findings suggest that poor olfaction is associated with multiple AD-related and other neurodegenerative processes.
Why it matters
In 1,545 older adults, poorer sense of smell was linked to higher levels of several Alzheimer's-related and neurodegeneration blood markers. This cross-sectional study shows an association only and cannot show whether smell loss causes or predicts disease.
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Whether or not neuropsychiatric symptoms (NPS) in advance of dementia are associated with Alzheimer's disease (AD) and/or other neurodegenerative dementias remains to be determined.
Why it matters
This study found that mild behavioral impairment before death was strongly associated with Alzheimer's disease pathology but not with other neurodegenerative dementias, and no significant associations were seen for Lewy body disease pathology. It examines associations with post-mortem pathology and does not test any treatment, cure, or prevention.
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Among 4712 participants (59% female; mean age, 74 years), 193 ischemic strokes and 769 dementia cases were ascertained over a median follow-up of 8.3 years.
Why it matters
In this cohort study, left atrial reservoir strain and NT-proBNP improved prediction of a combined outcome of ischemic stroke and dementia when added to a standard risk model. The authors support using left atrial reservoir strain to identify people at high risk of cerebrovascular events and dementia, but the study does not test any treatment, cure, or prevention.
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Among 463 ADNI participants with baseline MCI (mean age 72.6 ± 7.3 years, 43.4% female), the OSA PRS, adjusted for BMI, was significantly associated with MCI-to-AD progression.
Why it matters
A genetic risk score for obstructive sleep apnea was linked to higher risk of progressing from mild cognitive impairment to Alzheimer's, and to more amyloid deposition and cognitive decline, while risk scores for type 2 diabetes, coronary artery disease, major depression and BMI were not. The authors caution that the small sample size and lack of objective sleep apnea diagnosis limit interpretation, so this does not establish a treatment or prevention.
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It has been suggested that the diagnostic landscape of Alzheimer disease (AD) is undergoing a profound transformation, marked by a shift toward a biomarker-based approach, as proposed by the Revised Criteria for Diagnosis and Staging of Alzheimer's Disease.
Why it matters
This article argues that defining Alzheimer disease by biomarkers alone risks a category error and that more longitudinal data are needed to know the lifetime dementia risk in amyloid-positive and tau-positive people. It recommends keeping the criteria in the research domain for now and does not offer a treatment, cure or prevention.
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Alzheimer's disease (AD) has recently been associated with diverse cell states 1-11 , yet when and how these states affect the onset of AD remains unclear.
Why it matters
Using 1.65 million single-cell gene-activity profiles from the prefrontal cortex of 437 older people, this study mapped how brain cell populations shift with age and found two paths: one leading to Alzheimer's dementia and one to "alternative brain ageing." Its causal modelling pointed to two lipid-associated microglia groups — one linked to amyloid build-up, the other to amyloid's effect on tau — and an astrocyte group linked to tau's effect on cognitive decline. These are statistical links in brain tissue, not a tested treatment, test or cure.
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In the longitudinal analysis of p-tau181 trajectories of the AD+P group, the group of patients who showed incidence of psychosis over the course of follow-up (AD+P incident) demonstrated an associated increase in plasma p-tau181 levels compared with the group of patients who had psychosis at baseline (AD+P baseline) and showed an associated decrease in plasma p-tau181 levels (F4, 117 = 3.24; P = .01).
Why it matters
In this cohort of 752 people with Alzheimer's disease, the new appearance of psychosis was linked to rising plasma p-tau181 levels. This points to plasma p-tau181 as a possible biomarker for neuropsychiatric symptoms, not as a treatment or cure.
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Indeed, in our review, we observed a stage-dependent neuroinflammatory process in the AD brain.
Why it matters
This review notes that recent trials of anti-amyloid antibodies such as lecanemab and donanemab showed limited clinical benefits and a significant risk of serious adverse events. It describes a stage-dependent neuroinflammatory process in the Alzheimer's brain and discusses tracking inflammatory biomarkers for individualized treatment approaches.
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There are limited data regarding cerebrospinal fluid (CSF) and plasma biomarkers among patients with Cerebral Amyloid Angiopathy (CAA).
Why it matters
This review compared CSF and plasma biomarker levels in people with cerebral amyloid angiopathy against healthy controls and people with Alzheimer's disease. It is about improving diagnosis and distinguishing these conditions, not about treating or preventing Alzheimer's.
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In patients with early PD, CSF p-tau 181 and t-tau were low compared with those in controls and did not increase over 5 years of follow-up.
Why it matters
In 364 people with early Parkinson disease, spinal fluid p-tau181 and t-tau were lower than in controls and did not rise over 5 years of follow-up. This concerns Parkinson disease markers and reports no increase in these Alzheimer-related tau measures.
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These findings suggest that increases in certain plasma AD biomarkers are associated with NP in WLWH and WLWOH and may be associated with later onset of AD, and measuring these biomarkers could be a pivotal advancement in monitoring aging brain health and development of AD among women with and without HIV.
Why it matters
Among 307 women with and without HIV, several plasma Alzheimer's biomarkers were associated with neuropsychological performance, and women living with HIV performed worse on several cognitive measures at baseline. This is about biomarkers and cognitive associations, not about treating or preventing Alzheimer's disease.
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Treatment options for Alzheimer disease (AD) are limited and have focused mainly on symptomatic therapy and improving quality of life.
Why it matters
This cross-sectional study took the eligibility rules used in the lecanemab clinical trial and applied them to people with early Alzheimer's disease in the population-based Mayo Clinic Study of Aging. Its aim was to see how well those trial rules carry over to adults in the general population, which the authors say had not been studied. It looks at who could qualify for anti-amyloid treatment, not at whether the treatment works.
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We observed no differences in plasma AD biomarker levels between AA and NHW participants.
Why it matters
In a community sample of 267 African American and 268 non-Hispanic White adults, blood-test markers of Alzheimer's disease did not differ by self-reported race, including within each cognitive-status group (unimpaired vs impaired). Sex, chronic kidney disease and vascular risk factors, not race, were linked to differences in these markers, and apparent race-specific links to cognition disappeared once people with kidney disease were excluded. The authors conclude that health conditions like these should be taken into account when Alzheimer's blood tests are used in the general population; the study is about reading the tests, not about treatment or prevention.
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These results suggest that plasma biomarkers can augment detection of preclinical AD among asymptomatic individuals and improve the specificity of AD diagnosis.
Why it matters
This cross-sectional study evaluated plasma biomarkers for classifying Alzheimer's disease among adults of Caribbean Hispanic ethnicity. The results suggest that plasma biomarkers can help detect preclinical Alzheimer's disease in asymptomatic individuals and improve diagnostic specificity, but the available summary does not report the size or strength of these effects.
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Global PET amyloid burden was compared with regards to cognitive status, APOE ɛ4 status, sex, age, and estimated years to symptom onset.
Why it matters
This cross-sectional study found that amyloid PET changes were similar between people with autosomal dominant Alzheimer's disease and people with Down syndrome, supporting early amyloid dysregulation in Down syndrome. It is a diagnostic imaging study and does not report any treatment, cure, or prevention of Alzheimer's disease.
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Alzheimer's disease (AD) is a heterogeneous disorder with abnormalities in multiple biological domains.
Why it matters
Using brain and blood samples from 1,863 people, this study identified three molecular subtypes of Alzheimer's that differ in DNA methylation, RNA, proteins and metabolites. The authors say this taxonomy may point to distinct targets for prevention or treatment, but no treatment was tested.
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Blood-based markers (BBMs) have recently shown promise to revolutionize the diagnostic and prognostic work-up of Alzheimer's disease (AD), as well as to improve the design of interventional trials.
Why it matters
Alzheimer's Association recommendations on blood tests for Alzheimer's disease. For now they recommend blood biomarkers as pre-screeners for trial entry, with Alzheimer's status confirmed by PET or spinal fluid (CSF) testing, and cautious use in specialized memory clinics with confirmation where possible. More data are needed before they are used as stand-alone diagnostic tests or in primary care.
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Considering predementia stages, the number of persons with AD is much larger than conveyed in available literature.
Why it matters
By combining published prevalence studies in a model, this study estimated that worldwide about 32 million people have Alzheimer's dementia, 69 million are in the prodromal stage and 315 million in the preclinical stage — "416 million across the AD continuum, or 22% of all persons aged 50 and above". Most of these people do not have dementia, so the authors conclude the number of people with AD "is much larger than conveyed in available literature". The authors call the estimates "uncertain, especially for predementia stages in low- and middle-income regions where biomarker studies are missing"; the study counts people for planning and does not test any treatment, prevention or the risk of progressing to dementia.
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60/100
Neuroimaging and biofluid tau markers hold potential for optimising such clinical trials by augmenting participant selection, providing evidence of target engagement, and monitoring treatment efficacy.
Why it matters
This paper states that neuroimaging and biofluid tau markers hold potential for optimising clinical trials by augmenting participant selection, providing evidence of target engagement, and monitoring treatment efficacy. Major challenges to overcome include the high cost of tau-PET, partial sensitivity to detect early-stage Alzheimer's disease pathology, and off-target tracer binding.
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60/100
The neuropathologic changes underlying Alzheimer disease (AD) start before overt cognitive symptoms arise, but it is not well-known how they relate to the first subtle cognitive changes.
Why it matters
This study examined how amyloid beta, tau, and neurodegeneration relate to different cognitive domains in cognitively unimpaired adults. It is a cross-sectional observational study and does not test any treatment, cure, or prevention.
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Elecsys-derived CSF biomarkers detect AD neuropathologic changes with very high discriminative accuracy in vivo.
Why it matters
In this study, fully automated CSF biomarkers distinguished pathology-confirmed Alzheimer disease dementia from healthy controls and from non-Alzheimer dementias, and detected amyloid and tau pathology at autopsy. This is about diagnostic accuracy and does not test any treatment, cure, or prevention.
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To assess plasma phosphorylated tau181 (p-tau181) as a progression biomarker in Alzheimer's disease (AD), we examined longitudinal plasma p-tau181 of 1184 participants (403 cognitively normal (CN), 560 patients with mild cognitive impairment (MCI), and 221 with AD dementia) from Alzheimer's Disease Neuroimaging Initiative (ADNI).
Why it matters
In 1,184 participants, plasma phosphorylated tau 181 was higher at baseline in those with mild cognitive impairment and Alzheimer's dementia and increased over time across preclinical, prodromal, and dementia stages. This marker was also linked to abnormal cerebrospinal fluid biomarkers, amyloid accumulation, and hypometabolism on PET scans, suggesting it may help track disease progression.
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Neuropsychiatric symptoms (NPSs) are common in patients with Alzheimer's disease (AD) and are associated with accelerated cognitive impairment and earlier deaths.
Why it matters
This review describes which brain regions are damaged in people with Alzheimer's disease who have neuropsychiatric symptoms, and notes that most of these symptoms appear in the preclinical or mild cognitive impairment stage. It is a review of brain lesion patterns and does not test any treatment, cure, or prevention.
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This review presents an overview of the latest advances in the field of biomarkers for neurodegenerative diseases.
Why it matters
This review describes how PET scans and newer, cheaper blood tests can detect the amyloid-beta and tau changes of Alzheimer's disease. Better detection helps design clinical trials and could make diagnosis more widely available, but the review itself does not test a treatment.
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.
- The lower hippocampus global connectivity, the higher its local metabolism in Alzheimer disease
- Self-rated and informant-rated everyday function in comparison to objective markers of Alzheimer's disease
- Investigating the Impact of NMDA Receptor Organization and Biological Sex in the APPswe/PS1dE9 Mouse Model of Alzheimer’s Disease
- Presymptomatic cortical thinning in familial Alzheimer disease: A longitudinal MRI study
- APOE4 homozygosity represents a distinct genetic form of Alzheimer's disease
- Genetic Variants Associated With Alzheimer Disease in the 22 Arab Countries: A Systematic Review
- Hippocampal atrophy on MRI in frontotemporal lobar degeneration and Alzheimer's disease
- Neuroimaging Correlates of Cerebral Microbleeds: The ARIC Study (Atherosclerosis Risk in Communities)
- Pittsburgh plasma p-tau217: Classification accuracies for autosomal dominant and sporadic Alzheimer's disease in the community
- Economic evaluation of donepezil in moderate to severe Alzheimer disease