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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In postmortem investigations of patients with dementia of Alzheimer type (AD/SDAT) (n = 14) the brain weight was significantly reduced when compared to controls (n = 16).
Why it matters
This postmortem study of 14 patients with dementia of Alzheimer type found reduced brain weight and reduced concentrations of several neurotransmitters compared with 16 controls. It describes biochemical changes in the brain and reports no treatment, cure or prevention for Alzheimer's disease.
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Alzheimer's disease (AD) is responsible for 70% of dementia cases worldwide, with tau hyperphosphorylation and amyloid-β plaque accumulation representing its core pathological hallmarks.
Why it matters
Reviewing lab and clinical studies, the authors identified many non-coding RNAs, molecules that control gene activity, that regulate how mitochondria, the cell's power plants, work in Alzheimer's, including miR-140 and lncRNA NEAT1. Several were also found to be abnormal in patients. The authors say this research is at an early stage, but that these molecules are promising candidates for future biomarkers and treatments.
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The study aim is to investigate whether blood biomarkers (BBMs) of Alzheimer's disease (AD) pathology are associated with postoperative cognitive dysfunction (POCD) after cardiac surgery.
Why it matters
In 394 patients undergoing cardiac surgery, this study investigated whether preoperative Alzheimer's disease blood biomarkers were associated with cognitive decline 12 months after surgery. It addresses risk prediction for postoperative cognitive decline and does not test treatment, cure, or prevention of Alzheimer's disease.
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= 0.015). In this autopsy-confirmed cohort, seizure susceptibility was associated with advanced tau pathology and CAA in AD.
Why it matters
In this autopsy-confirmed cohort, seizure susceptibility was associated with advanced tau pathology and CAA in Alzheimer's disease, while exploratory analyses in DLB suggested a possible association with vascular pathology. These findings support distinct pathologic contributions to seizures across dementia subtypes, but the use of advanced-stage samples may limit generalizability to earlier disease stages.
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= 0.007) in AD-signature regions and a numerically higher burden of vascular risk factors.
Why it matters
In a Chinese memory clinic cohort, clinical and biological staging under the 2024 criteria often disagreed among amyloid-positive individuals, and plasma p-tau217 rose stepwise across tau PET stages. These findings support the clinical relevance of the revised staging framework for diagnosis, not a treatment or cure.
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Impaired lung function (ILF) has been associated with cognitive decline and dementia risk in multiple cohorts, yet the role of circulating Alzheimer disease (AD) biomarkers in this relationship is not well understood.
Why it matters
In 4,072 participants, impaired lung function was associated with higher blood biomarkers of AD/ADRD, and these biomarkers statistically accounted for part of the link between impaired lung function and incident dementia. This is about understanding risk factors and markers, not about a treatment or cure.
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In total, 881 (21.6%) participants had ILF and 272 (6.8%) participants developed dementia.
Why it matters
Impaired lung function was associated with a higher risk of dementia and with higher blood NfL and p-Tau181, though these markers explained only modest portions of the link. The authors call for further investigation into biological pathways, so this does not offer a treatment, cure or prevention.
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BackgroundSeveral monoclonal antibodies designed to slow cognitive and functional decline in individuals with early Alzheimer's disease (AD) have been recently approved.
Why it matters
At a willingness-to-pay threshold of $100,000 per QALY, all included studies found memantine cost-effective and more than half reported cost-effectiveness for donepezil, rivastigmine and galantamine, while aducanumab, lecanemab and donanemab were not cost-effective in any study. These conclusions come from economic models, not from new trials of whether these drugs work.
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Non-elevated plasma p-tau181 results impacted the diagnosis and use of amyloid PET imaging in a memory clinic.
Why it matters
Plasma p-tau181 testing raised clinicians' diagnostic confidence, but changes in diagnosis and management were below the study's 30% threshold for clinical significance. This suggests limited impact on care in this memory clinic, and it is not a treatment or cure.
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Disruptions in GABAergic activity and alterations in gamma oscillations are key pathological features of AD associated with amyloid-beta (Aβ) plaques.
Why it matters
This review of animal and human studies describes disruptions in GABAergic activity and gamma oscillations as key features of Alzheimer's disease associated with amyloid-beta plaques. It discusses therapeutic neuromodulatory insights but does not report a proven treatment or cure.
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After deduplication and screening of 8893 records, we included 109 studies describing a wide array of wearable or portable DHTs that obtained digital biomarkers.
Why it matters
This scoping review of 109 studies found a growing evidence base for wearable or portable digital biomarkers in early Alzheimer's disease, most commonly rest/activity, speech, and gait. However, few studies reported outcomes associated with diagnosis or prognosis, representing a knowledge gap, and this does not treat, cure, or prevent Alzheimer's disease.
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We included 1179 CU subjects (n = 474 females (40%), 70.9 ± 4.5 years old) of European descent who had pTau217 and PACC.
Why it matters
In cognitively unimpaired older adults, a microglia-specific Alzheimer polygenic risk score predicted a longitudinal increase in plasma tau and faster cognitive decline. The findings suggest that much of the microglial effect on cognitive decline may occur through accelerated tau pathology, but no treatment is tested.
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274 participants [average age 75.9 (SD 5.8); 57% women; 13% self-identified as Black] were offered their research results and 40% declined.
Why it matters
In this longitudinal cohort, 40% of participants offered their research biomarker results declined to learn them, with Black participants and those with a parental history of Alzheimer dementia more likely to decline. Qualitative interviews found reasons including that knowing would be a burden and the uncertainty of results.
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Globally, the age-standardized incidence rates (ASIR) remained relatively steady.
Why it matters
This global analysis found that while age-standardized incidence rates of Alzheimer's disease and other dementias stayed relatively steady, the total number of cases rose 141.25% to 9,837,056 in 2021. It calls for strengthened surveillance and management of adults over 60 and targeted public health policies to address the growing burden.
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Significant improvement over time was observed in aggregated domain specific composite scores of episodic and semantic memory and spatial abilities.
Why it matters
This randomized controlled trial found no significant interaction between groups and timepoints for computerized cognitive training, no significant changes in grey matter volume, and no moderating effect of amyloid levels, though cognitive and subjective improvements were seen over time. It concludes there were no specific advantages of the three-month intervention on cognitive or biological outcomes, while noting high adherence and suggesting inclusion of cognitive training in multicomponent interventions.
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In the HELIAD sample, among 618 cognitively healthy participants (mean age 73.37 years, 58.4% female), followed for 2.92 ± 0.80 years, 73 developed AD/aMCI.
Why it matters
A genetic score for plasma tau levels was associated with a higher risk of developing Alzheimer dementia or mild cognitive impairment in two large samples. The effect appeared stronger in women and younger participants, but the study does not show that this score can prevent or treat the disease.
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Our results highlight the prognostic value of biological AD staging.
Why it matters
This study found that biological Alzheimer's disease staging, based on amyloid and tau PET, predicted progression to mild cognitive impairment and dementia better than amyloid PET status, tau PET status, or demographic information alone. It does not test a treatment or cure, but it suggests this staging may help identify who is at higher risk of decline.
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The study included 25 patients with iCAA (age, 44±11 years), 31 patients with sCAA (age, 75±5 years), 28 patients with AD (age, 71±8 years) and 30 controls (age, 72±8 years) from 9 case descriptions and 1 cohort study.
Why it matters
Comparing cerebrospinal fluid markers, this study found phosphorylated tau concentrations in iatrogenic CAA were not significantly different from controls, unlike in sporadic CAA and Alzheimer's disease. This led to a hypothesis about how iatrogenic CAA differs, but it is a biomarker observation with no treatment implications.
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A decline in TMT was associated with worse cognitive function, increased cerebral tau deposition and impaired functional performance.
Why it matters
This study found that thinner temporal muscle thickness was associated with worse cognitive function, higher brain tau deposition, and impaired functional performance in Chinese adults. The link between temporal muscle thickness and cognitive scores remained significant in people with mild cognitive impairment but not in those with Alzheimer's disease.
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This comprehensive review examines the integration of Quantitative Electroencephalography (qEEG) and Artificial Intelligence (AI) in the detection and diagnosis of Alzheimer's Disease (AD).
Why it matters
This review reports that combining qEEG with AI achieved high diagnostic accuracy for detecting Alzheimer's disease in the studies examined. It addresses detection and diagnosis only, and notes ongoing challenges in data quality, computing resources and standardisation; it does not report any treatment or cure.
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Higher ARTS score was associated (all ps < 0.01) with incident MCI (hazard ratio [HR] = 1.29), dementia (HR = 1.33), and stroke (HR = 1.52) and with diastolic/systolic blood pressure, self-reported hypertension, claudication, congestive heart failure, smoking, and glomerular filtration rate in the combined sample.
Why it matters
Higher ARTS score, described as an in vivo marker of cerebral arteriolosclerosis, was associated with incident mild cognitive impairment, dementia, and stroke, and with vascular risk factors. This points to a possible marker of risk related to blood vessel disease, but it does not show a treatment or cure.
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This approach offers a sensitive method for identifying individuals at high risk for AD-related cognitive decline.
Why it matters
In 954 amyloid-positive cognitively unimpaired people, combining a digital cognitive assessment with plasma p-tau217 improved prediction of cognitive decline over the next 5 years better than either measure alone. This is about early detection and risk prediction, not about treating, curing or preventing Alzheimer's disease.
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The defining pathological features of Alzheimer disease (AD) may also be contributing factors in other dementias.
Why it matters
This large cross-sectional study examined how common amyloid and tau changes, measured in spinal fluid, are across a broad range of dementias and how they relate to clinical progression. It is an observational study and does not test any treatment or cure.
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Alzheimer's disease (AD) is a complex and progressive neurodegenerative disorder with a continuum of stages ranging from preclinical/asymptomatic phase to severe dementia.
Why it matters
This review describes current treatment strategies for the Alzheimer's disease spectrum, including anti-amyloid immunotherapies such as lecanemab and donanemab that slow cognitive decline in early-stage disease, and standard symptomatic treatments. It reports that strategies targeting tau pathology and neuroinflammation are still under investigation, so no cure or prevention is established.
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In AD cases, pTau181 and ApoE4 levels were elevated, and the Aβ1-42/1-40 ratio was reduced.
Why it matters
This study found that blood levels of pTau181 and ApoE4 were elevated and the Aβ1-42/1-40 ratio was reduced in Alzheimer's disease, and that combining markers improved distinguishing Alzheimer's from healthy controls. These are diagnostic findings only and say nothing about treating, curing, or preventing the 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.
- Morphological and biochemical analyses of amyloid plaque core proteins purified from Alzheimer disease brain tissue
- Atrophy patterns in cerebral amyloid angiopathy with and without cortical superficial siderosis
- Apolipoprotein E Genotype and Sex Risk Factors for Alzheimer Disease: A Meta-analysis
- A blood-based predictor for neocortical Aβ burden in Alzheimer's disease: results from the AIBL study
- Associations Between CSF Markers of Inflammation, White Matter Lesions, and Cognitive Decline in Individuals Without Dementia
- APOE alleles predict the rate of cognitive decline in Alzheimer disease: a nonlinear model
- Centenarian controls increase variant effect sizes by an average twofold in an extreme case-extreme control analysis of Alzheimer's disease
- Late onset Alzheimer's disease genetics implicates microglial pathways in disease risk
- A multivariate approach to identify association between peripheral blood DNA methylation and cerebrospinal fluid biomarkers of Alzheimer disease
- Nonlinear Association Between Cerebrospinal Fluid and Florbetapir F-18 β-Amyloid Measures Across the Spectrum of Alzheimer Disease