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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Lecanemab is a humanized monoclonal antibody that binds soluble brain amyloid-β protein, promoting its removal and slowing the underlying process of Alzheimer disease. 1 This mechanism aligns with the amyloid hypothesis, a debated model of Alzheimer disease pathogenesis.1 Only patients with mild cognitive impairment (MCI) or mild dementia due to Alzheimer disease are eligible for lecanemab treatment.
Why it matters
Lecanemab is a monoclonal antibody that binds soluble brain amyloid-β and slows the underlying disease process, and it is approved in Canada for patients with mild cognitive impairment or mild dementia due to Alzheimer disease. However, Canada's Drug Agency and Quebec's health agency recommended against public reimbursement, and eligibility requires APOE genotyping and confirmation of amyloid positivity.
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BackgroundLecanemab is the first approved disease-modified therapy in Japan for patients with mild cognitive impairment (MCI) due to Alzheimer's disease (AD) or mild AD dementia (AD-D).ObjectiveThis study aims to evaluate the social value of lecanemab in Japan.
Why it matters
In this cost-effectiveness model, lecanemab added to standard of care extended time spent in early Alzheimer's disease and produced incremental cost-effectiveness ratios of JPY 8.5 million per QALY for mild cognitive impairment due to Alzheimer's disease and JPY 7.9 million per QALY for mild Alzheimer's disease dementia. These are modelled estimates of value that varied greatly depending on the perspectives and methods used, not direct evidence of clinical benefit.
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Alzheimer's disease (AD) is one of the most common neurological disorders affecting older adults, with approximately 7.2 million cases only in the United States.
Why it matters
This review examines whether combining magnetic resonance spectroscopy, diffusion tensor imaging, and structural MRI can detect metabolic, microstructural, and anatomical brain changes before cognitive symptoms appear in Alzheimer's disease. It does not test a treatment or cure, but it suggests these imaging methods may help with early diagnosis and predicting progression from mild cognitive impairment.
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Alzheimer's disease (AD) is the most prevalent cause of dementia and can be conceptualized as a tauopathy initiated by the accumulation of amyloid-β (Aβ) in the brain.
Why it matters
This review highlights lysosomes as key sites of intracellular amyloid-beta toxicity and points to several molecular pathways as possible targets for future Alzheimer's drugs. It summarizes ongoing research rather than reporting a proven treatment or cure.
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Alzheimer's disease and related dementias (ADRD) affects millions of patients worldwide and is a leading cause of morbidity in older adults.
Why it matters
This review describes a cycle in which dementia raises the risk of urinary tract infection and related delirium, and delirium then speeds up cognitive and functional decline. It discusses prevention and management strategies and possible biological mechanisms, but reports no cure.
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The proposed Deep-CNN and attention model focuses the model capacity on diagnostically relevant regions.
Why it matters
This study describes a deep convolutional neural network with an attention mechanism that classified Alzheimer's disease from MRI images with 97% accuracy, higher than several comparison methods. The attention maps aligned with known Alzheimer's disease biomarkers, which the authors say provides clinically useful regional explanations.
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MR analysis identified phosphatidylinositol (PI) (16:0_20:4), phosphatidylcholine (PC) (16:0_22:4) and sterol ester (SE) (27:1/15:0) as risk factors for AD.
Why it matters
This genetic study identified specific phosphatidylinositol, phosphatidylcholine, and sterol ester lipid subtypes as risk factors for Alzheimer's disease, and several phosphatidylinositol and triacylglycerol subtypes as protective. These findings suggest lipid metabolism is causally involved and highlight potential lipid-based therapeutic targets, but no treatment was tested.
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These findings suggest that adherence to the MIND diet may support nutrition and psychological well-being in AD and highlight the value of integrating nutrition-based approaches into dementia care.
Why it matters
In this small case-control study of 30 Alzheimer's patients and 30 healthy controls, higher MIND diet adherence was associated with lower malnutrition and depression scores among patients. The study cannot show whether the diet prevents or treats Alzheimer's disease.
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Controversial relationship of rheumatoid arthritis (RA) with Alzheimer disease (AD) risk has been reported in previous research.
Why it matters
This genetic analysis found that rheumatoid arthritis had a positive causal effect on the risk of developing Alzheimer's disease, while Alzheimer's disease did not affect rheumatoid arthritis risk. This suggests a possible link between the two conditions, but the finding comes from statistical genetic methods and does not directly lead to a treatment or cure.
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A total of 144 surveys were collected from VA clinicians at baseline and during audit-feedback sessions (Table).
Why it matters
This survey of VA clinicians identified barriers to diagnosing Alzheimer's disease and to delivering disease-modifying treatments, and led to process changes such as a cognitive testing workflow. It does not test a treatment, cure, or prevention for Alzheimer's disease.
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After adjusting for age, sex, race/ethnicity, education, APOE ε4, and physical activity, a greater multimorbidity burden (per 3 additional conditions) was associated with worse overall cognition (standardized β = -0.074, 95%CI -0.104 to -0.043) and biomarkers indicative of greater AD pathology, neurodegeneration, and SVD (Figure 1).
Why it matters
This pathway analysis found that a greater multimorbidity burden was associated with worse overall cognition and with biomarkers of greater Alzheimer disease pathology, neurodegeneration, and small vessel disease. The association between multimorbidity and worse cognition was primarily mediated by neurodegeneration and partially by Alzheimer disease pathology.
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Both 17αE2 and FMD independently reduced AD neuropathology in the EFAD mice, in an APOE-dependent manner.
Why it matters
In aged EFAD mice, two longevity-related treatments, 17αE2 and a fasting-mimicking diet, each reduced Alzheimer's-like neuropathology, with the strongest effects in mice carrying the APOE4 genotype. This is animal research, and combining the two treatments gave no extra benefit, so it does not yet show that either approach treats or prevents Alzheimer's disease in people.
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Participants did not differ significantly based on sex.
Why it matters
This study found that decreased T-cell receptor diversity was only marginally associated with having Alzheimer's disease or mild cognitive impairment, and the association was not significant after adjusting for age and sex. These are preliminary findings, and the work is ongoing to develop predictive models for diagnosis.
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After a 30-minute educational session, participants showed greater positivity toward an ADRD diagnosis and increased confidence in discussing early detection.
Why it matters
Among 25 rural providers and administrators surveyed, 75% were not ordering ADRD biomarker testing and 62% felt unqualified to order biomarkers, though a 30-minute educational session improved confidence. This describes barriers to using biomarkers in rural practice, not a treatment, cure, or prevention.
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AD patients exhibited a significantly higher prevalence of APOE e3/e4 and e4/e4 genotypes compared to DLB and HC (p <0.001).
Why it matters
This study found that metabolomic biomarkers, combined with APOE, improved classification accuracy for distinguishing Alzheimer's disease from dementia with Lewy bodies. It is a diagnostic study only and does not test any treatment, cure or prevention, and the authors note larger cohorts are needed.
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Cognitive impairment associated with Aβ positivity and low tau (A+T‐) is linked to mixed AD.
Why it matters
Among 77 individuals with autopsy data, those who were Aβ positive but tau biomarker negative (A+T-) were as cognitively impaired as A+T+ individuals, and this group was linked to significant non-Alzheimer's disease neuropathologies. The findings suggest that cognitive impairment with Aβ positivity and low tau may often be due to mixed or non-Alzheimer's pathologies, which matters for interpreting biomarker results but does not offer a treatment or cure.
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After adjusting for age, sex, race/ethnicity, education, APOE ε4, and physical activity, a greater multimorbidity burden (per 3 additional conditions) was associated with worse overall cognition (standardized β =-0.074, 95%CI -0.104 to -0.043) and biomarkers indicative of greater AD pathology, neurodegeneration, and SVD (Figure 1).
Why it matters
In dementia-free individuals, a greater burden of multiple medical conditions was associated with worse overall cognition, and this link was mainly mediated by neurodegeneration (74%) and partly by Alzheimer's pathology (22%). The findings suggest that managing multiple health conditions may matter for cognition, but this is an observational study and does not test any treatment or cure for Alzheimer's disease.
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Positron emission tomography (PET) allows for minimally invasive in vivo localization of amyloid and tau deposition, and visualization of glucose metabolism using amyloid PET, tau PET, and FDG PET.
Why it matters
This review of 76 published studies found that early-phase amyloid and tau PET scans were consistently good at indicating neurodegeneration, and that limited research suggests a single PET scan might also help infer amyloid and tau status. The authors describe these initial results as promising but say they still need to be validated.
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MIND scores were significantly lower in the AD group (P < 0.001).
Why it matters
In this study, higher MIND diet adherence was associated with better cognition, lower dementia severity, fewer mood symptoms and greater daily functioning in people with Alzheimer's disease. EEG markers partially mediated these associations, but the study cannot show that the diet causes these improvements.
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Alzheimer's disease (AD) is the most common cause of dementia in older adults, marked by a gradual and irreversible deterioration of cognitive abilities, including memory and thinking skills.
Why it matters
This review focuses on how the systems that maintain protein integrity and the brain's inflammatory response interact in Alzheimer's disease, and on treatments and biomarkers being studied for these processes. It summarizes existing research rather than reporting a new treatment that works.
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Alzheimer's Disease (AD) is the most common dementia, affecting mainly older adults, particularly over 65.
Why it matters
This review describes how microglia can protect against Alzheimer's by clearing amyloid-beta, but that disrupted homeostasis can trigger harmful microglial activation, inflammation, synapse loss and neuronal damage. It frames inflammation as a possible therapeutic avenue but reports no tested treatment or outcome.
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Alzheimer disease (AD) polygenic risk scores (ADPRS) built from cell-type (ct) specific genetic variants can be used to infer cell-type contributions to AD.
Why it matters
Cell-type-specific Alzheimer's disease polygenic risk scores derived from single-nuclei data were associated with tau tangle burden, neuritic plaque burden, and MMSE score. This is a genetic and molecular analysis and does not test any treatment, cure, or prevention.
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From 1990 to 2021, the incidence, prevalence, and DALYs of ADOD have significantly risen both globally and in China, with the growth rates in China notably surpassing the global average.
Why it matters
The number of new cases, existing cases, and disability from Alzheimer's disease and other dementias rose significantly from 1990 to 2021, with China's growth outpacing the global average. The risk increased exponentially with age, and women were disproportionately affected.
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37/100
Promising therapeutic interventions that target the underlying pathophysiology are changing the landscape of Alzheimer's disease (AD) research.
Why it matters
This paper reports on a meeting about how health systems can identify patients early and deliver emerging Alzheimer's therapies safely. It does not present new treatment, cure, or prevention results, but describes challenges in the care pathway that must be addressed.
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Alzheimer's disease (AD) is the most common cause of dementia.
Why it matters
Using existing single-nuclei datasets, this analysis identified an astrocyte subtype that may promote amyloid beta and neurofibrillary tangle accumulation through specific genes. This is a data analysis study, so it does not provide a treatment or prevention for Alzheimer's disease.
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.
- Evaluation of Plasma Biomarkers for A/T/N Classification of Alzheimer Disease Among Adults of Caribbean Hispanic Ethnicity
- A review on Alzheimer's disease pathophysiology and its management: an update
- Prevalence of Alzheimer's disease and vascular dementia: association with education. The Rotterdam study
- Longitudinal assessment of cognitive decline and resilience in high-level Alzheimer disease neuropathologic change
- Fractionating verbal episodic memory in Alzheimer's disease
- Soluble amyloid beta-protein is a marker of Alzheimer amyloid in brain but not in cerebrospinal fluid
- Dissociation of Down syndrome and Alzheimer's disease effects with imaging
- Clinical predictors of progression to Alzheimer disease in amnestic mild cognitive impairment
- Genetic variations underlying Alzheimer's disease: evidence from genome-wide association studies and beyond
- Clinical aspects of melatonin intervention in Alzheimer's disease progression