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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Participants age 60-85 years deemed cognitively unimpaired were disclosed an elevated or not elevated brain amyloid result by a certified clinician.
Why it matters
Among 3378 cognitively unimpaired participants, those told they had elevated brain amyloid showed higher concerns about Alzheimer's disease and mild distress after disclosure compared with those told their result was not elevated. The authors note sample bias must be considered, but the findings suggest amyloid disclosure increased perceived risk and caused mild distress.
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With the increase in large multimodal cohorts and high-throughput technologies, the potential for discovering novel biomarkers is no longer limited by data set size.
Why it matters
This review discusses how artificial intelligence and machine learning may help discover novel biomarkers for Alzheimer's disease and dementia, while noting challenges such as lack of diversity in data sets and poor reporting. It concerns biomarker discovery methods and does not test any treatment, cure, or prevention for Alzheimer's disease.
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Vascular cognitive impairment and dementia (VCID) is commonly caused by vascular injuries in cerebral large and small vessels and is a key driver of age-related cognitive decline.
Why it matters
This review describes cerebral small vessel disease as a common cause of vascular cognitive impairment and dementia, which frequently coexists with Alzheimer's disease. It states that the current main approach is to control vascular risk factors such as hypertension, dyslipidemia, diabetes, and smoking, and that causal therapeutic strategies have not been established.
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56/100
Genetic studies of Alzheimer disease (AD) have prioritized variants in genes related to the amyloid cascade, lipid metabolism, and neuroimmune modulation.
Why it matters
This study used brain tissue to map how different Alzheimer's risk genes affect specific cell types, finding distinct changes such as dysregulated autophagy in TREM2-related oligodendrocytes and signs of ferroptosis in APOE4 neurons. It provides a resource for understanding cellular diversity in Alzheimer's but does not test any treatment or prevention.
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Alzheimer's disease (AD) is the leading cause of dementia in elderly people.
Why it matters
This review describes how hyperphosphorylated tau accumulates and causes neuronal dysfunction across tauopathies including Alzheimer's disease and frontotemporal dementia, and discusses drugs targeting phosphorylated tau. It is a summary of existing research rather than a new treatment, cure or prevention result.
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The extent to which the pathophysiology of autosomal dominant Alzheimer's disease corresponds to the pathophysiology of 'sporadic' late onset Alzheimer's disease is unknown, thus limiting the extrapolation of study findings and clinical trial results in autosomal dominant Alzheimer's disease to late onset Alzheimer's disease.
Why it matters
Comparing 292 autosomal dominant Alzheimer's disease carriers with 559 late-onset participants, biomarker profiles were similar and both groups showed accelerated cognitive and brain volume decline after symptom onset. This supports a shared pathophysiology between the two forms and does not report a treatment, cure or prevention.
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The classic pathologic hallmarks of Alzheimer's disease (AD) are amyloid plaques and neurofibrillary tangles (AD neuropathologic changes, or ADNC).
Why it matters
This study found that some gene variants linked to Alzheimer's-type dementia are also associated with other brain pathologies besides the classic amyloid plaques and tangles. It does not show that targeting these genes prevents or treats dementia.
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Two genetic variants in strong linkage disequilibrium (rs9536314 and rs9527025) in the Klotho (KL) gene, encoding a transmembrane protein, implicated in longevity and associated with brain resilience during normal aging, were recently shown to be associated with Alzheimer disease (AD) risk in cognitively normal participants who are APOE ε4 carriers.
Why it matters
This analysis combined large multi-center cohorts to examine whether Klotho heterozygosity affects Alzheimer disease risk, following earlier findings that heterozygous carriers had lower risk. It is a genetic association study and does not establish any treatment, cure or prevention.
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56/100
Among patients with cognitive symptoms, larger choroid plexus volume was associated with severity of cognitive impairment in the Alzheimer disease spectrum.
Why it matters
In 532 patients with cognitive symptoms, greater choroid plexus volume was found in those with more severe impairment, and some patients also had permeability and susceptibility measurements. This is a retrospective observational study, so it shows an association only and cannot prove that the choroid plexus causes Alzheimer's or that targeting it would help.
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The implication of gut microbiota in the control of brain functions in health and disease is a novel, currently emerging concept.
Why it matters
This review suggests that gut microbiota may affect brain function indirectly by influencing microglia and neuroinflammation, which could in turn affect synapses. These ideas are still emerging and no treatment or prevention for Alzheimer's disease is established here.
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Transactive response DNA binding protein of 43 kDa (TDP-43) is an intranuclear protein encoded by the TARDBP gene that is involved in RNA splicing, trafficking, stabilization, and thus, the regulation of gene expression.
Why it matters
This review reports that TDP-43 inclusions are found in up to 57% of Alzheimer's disease cases and are associated with more severe cognitive impairment. It does not test any treatment or prevention, so it has no direct implications for treating, curing, or preventing Alzheimer's disease.
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56/100
Individuals with early AD show heterogeneity in disease progression, which increases when stratifying on risk factors associated with progression.
Why it matters
This simulation study found that individual cognitive trajectories in early Alzheimer's disease are highly variable, producing wide ranges of possible effect sizes in trials. The results of recent anti-amyloid trials mostly fell within these ranges, meaning the study does not show that any treatment works.
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The number of people with clinical AD will increase as the "baby boom" generation reaches older ages, exerting a strong upward influence on disease burden.
Why it matters
Using data from 10,342 participants, the authors estimate that 6.07 million people in the US were living with clinical Alzheimer's disease in 2020, rising to 13.85 million in 2060. Prevalence in 2020 was 10.0% among non-Hispanic Whites, 14.0% among Hispanics and 18.6% among non-Hispanic Blacks.
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We examined whether sarcopenia is associated with the occurrence of late-life cognitive impairment.
Why it matters
In 1175 nondemented older adults, sarcopenia was associated with incident Alzheimer's dementia, mild cognitive impairment and cognitive decline. This is an observational association study and does not report any treatment, cure or prevention for Alzheimer's disease.
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56/100
DCTclock discriminates between diagnostic groups and improves upon traditional cognitive tests for detecting biomarkers of amyloid and tau pathology in CN older adults.
Why it matters
In 300 participants, a digital clock-drawing test discriminated diagnostic groups well and, among clinically normal older adults, its scores were associated with greater amyloid and tau burden on PET. This suggests a simple test may help detect early Alzheimer pathology, but it is a diagnostic association study and does not show any treatment or prevention effect.
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Intimate metabolic host-microbiome crosstalk regulates immune, metabolic, and neuronal response in health and disease, yet remains untapped for biomarkers or intervention for disease.
Why it matters
In a small cohort of 77 people, this study found differences in gut microbial metabolites, including tryptophan metabolites and short-chain fatty acids, between Alzheimer's disease, amnestic MCI, and healthy controls. It suggests a possible target for microbiota or dietary intervention, but no treatment was tested.
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Brain amyloid-beta (Aβ) plaques, a hallmark of the pathophysiology of Alzheimer's disease, have been associated with frailty.
Why it matters
This study looked at whether the plasma Aβ42/40 ratio predicted frailty over time in 477 community-dwelling older adults from the MAPT trial. It concerns frailty rather than Alzheimer's treatment, so it does not show how to treat, cure or prevent the disease.
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56/100
EPVS are related to SVD, also in early disease stages, but the lack of correlation with cognition suggests that their importance is limited.
Why it matters
In 778 study participants, enlarged perivascular spaces in several brain regions were associated with white matter lesion volume and, in the hippocampus, with hippocampal atrophy, but no associations were found with cerebrospinal fluid Alzheimer's markers, neuroinflammatory markers, vascular risk factors or cognitive tests. The study describes associations with small vessel disease markers and does not test any treatment, cure or prevention.
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Among dementia-like diseases, Alzheimer disease (AD) and vascular dementia (VD) are two of the most frequent.
Why it matters
Using MRI features from 60 subjects, this study found that machine learning algorithms had high discriminant power to classify Alzheimer disease versus vascular dementia, and the approach was then used to predict disease prevalence in 15 patients with a mixed profile. This is a diagnostic classification study and does not test any treatment, cure or prevention.
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Type I interferon (IFN) is a key cytokine that curbs viral infection and cell malignancy.
Why it matters
This study found a type I interferon-stimulated gene signature in the brains of multiple mouse models of Alzheimer's disease and in normal mouse brain challenged with amyloid fibrils, and reports that this response drives neuroinflammation and synapse loss. It is largely animal and in-vitro work and reports no treatment, cure or prevention for people.
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Alzheimer's disease (AD) is a progressive and irreversible brain degenerative disorder.
Why it matters
A deep learning method was developed to automatically segment the hippocampus and classify Alzheimer's disease from MRI scans. This is a technical tool for diagnosis and does not provide a treatment or cure.
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Short-term memory dysfunction is a key early feature of Alzheimer's disease (AD).
Why it matters
This longitudinal study in psychiatric patients identified blood gene expression biomarkers that track short-term memory. It suggests possible early detection approaches but does not provide a treatment or cure.
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D-CAA M + showed greater age-dependent FLR PiB retention (p - , and serially imaged asymptomatic M + demonstrated greater longitudinal increases (p = 0.004).
Why it matters
Amyloid PET detected vascular amyloid in carriers of the Dutch-type hereditary cerebral amyloid angiopathy mutation, and retention increased over time in asymptomatic carriers. This shows the imaging can track vascular amyloid in this rare inherited condition, but it does not test any treatment or prevention.
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Alzheimer's disease is a progressive neurodegenerative disease most often associated with memory deficits and cognitive decline, although less common clinical presentations are increasingly recognized.
Why it matters
This review describes the neuropathological diagnosis of Alzheimer's disease, noting that amyloid plaques and neurofibrillary tangles are still required for a pathological diagnosis and that there remain no effective treatment options for the great majority of patients. It also notes that Alzheimer's disease is a mixed proteinopathy frequently associated with other age-related processes, which confounds efforts to develop effective diagnostic tools and disease-modifying therapies.
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The deep-learning time-to-event model predicted individual subjects' progression to AD dementia with a concordance index of 0.762 on 439 Alzheimer's Disease Neuroimaging Initiative testing MCI subjects with follow-up duration from 6 to 78 months (quartiles: [24, 42, 54]) and a concordance index of 0.781 on 40 Australian Imaging Biomarkers and Lifestyle Study of Aging testing MCI subjects with follow-up duration from 18 to 54 months (quartiles: [18, 36, 54]).
Why it matters
This deep learning model predicted progression from mild cognitive impairment to Alzheimer's dementia from hippocampal MRI data, with a concordance index of 0.762 in one testing group and 0.781 in another. It is a prognostic tool for identifying likely progressors, not a treatment or cure.
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.
- Neuroinflammation and fractalkine signaling in Alzheimer's disease
- Cataract Aggravates Alzheimer-Like Pathologies and Cognitive Deficits in an APP/PS1 Mouse Model
- Clinical and attitudinal outcomes of a personalized, multimodal lifestyle intervention for Alzheimer's disease prevention in high-risk, cognitively normal older adults in north Alabama: A pilot study
- Neuroinflammation in Alzheimer's Disease: Current Progress in Molecular Signaling and Therapeutics
- The effects of mosaicism on biological and clinical markers of Alzheimer's disease in adults with Down syndrome
- Trajectory of plasma lipidome associated with the risk of late-onset Alzheimer's disease: a longitudinal cohort study
- Development of Alzheimer disease in Down syndrome individuals
- Plasma biomarkers distinguish Boston Criteria 2.0 cerebral amyloid angiopathy from healthy controls
- Modular machine learning for Alzheimer's disease classification from retinal vasculature
- Glial activation and inflammation along the Alzheimer's disease continuum