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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Higher glial fibrillary acidic protein (GFAP) was associated with higher depressive symptoms.
Why it matters
In a large community cohort, higher plasma GFAP was associated with more depressive symptoms, while amyloid beta 42/40 ratio, phosphorylated tau181 and neurofilament light chain were not. This cross-sectional finding links a marker to symptoms but does not show any treatment or prevention effect.
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A higher DMV score was significantly associated with increased likelihoods of MCI (OR=1.19; 95%CI=1.06‒1.34) and amnestic mild cognitive impairment (aMCI) (1.21; 1.06‒1.37), and lower scores in MMSE (-0.01; -0.02‒0.00; p = 0.041), global cognition (-0.05; -0.08‒-0.03), memory (-0.06; -0.10‒-0.02), verbal fluency (-0.05; -0.08‒-0.02), attention (-0.04; -0.07‒-0.01), and executive function (-0.06; -0.10‒-0.03).
Why it matters
In dementia-free older adults in rural China, a higher deep medullary vein score was associated with increased likelihood of mild cognitive impairment and lower scores in several cognitive domains, as well as a lower plasma amyloid-β42/amyloid-β40 ratio. This cross-sectional study suggests vein abnormalities are linked to cognitive function and Alzheimer's pathology, but it cannot show cause and effect and does not test any treatment.
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The advent of amyloid-β (Aβ) and tau PET imaging has revolutionized Alzheimer disease (AD) research, enabling in vivo detection of hallmark pathologies and transforming both diagnosis and therapeutic development.
Why it matters
This review describes how amyloid and tau PET imaging were used in clinical trials of approved anti-amyloid therapies, including for participant selection and treatment monitoring. It discusses how PET quantification could support decisions about eligibility, risk stratification, and treatment duration, but does not present new treatment results.
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< 0.035), consistent with a neurodegenerative pattern.
Why it matters
This study found that platelet aggregation was linked to PET and MRI markers of Alzheimer's disease pathology as early as midlife in participants of the Framingham Heart Study. The authors say these findings support further investigation of platelet-mediated mechanisms in Alzheimer's disease pathogenesis.
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Our findings suggest that disease progression follows a stage-dependent MVD pattern that can identify at-risk regions.
Why it matters
This study suggests that metabolic and vascular dysfunction in the brain varies by sex and disease stage and could serve as an early diagnostic tool for Alzheimer's disease. It may help improve patient monitoring, stratification, and therapeutic testing, but the findings are based on imaging and analytical methods that require further validation.
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The patterns of FDG decline are distinct in these 2 genetically determined forms of AD.
Why it matters
This cross-sectional imaging study found that brain glucose metabolism was substantially lower in people with Down syndrome than in neurotypical familial controls, even 20 years before expected symptom onset, with patterns distinct from autosomal dominant Alzheimer's disease. It describes a biomarker difference and does not test any treatment, cure or prevention.
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46/100
The mean (SD) age of participants was 70.57 (8.00) years, with 179 (42.9 %) females.
Why it matters
This cross-sectional study found that blood C-reactive protein levels had non-linear, U-shaped relationships with Alzheimer's disease biomarkers, with different effects at low and high levels. Because it is cross-sectional, it cannot show whether these relationships are causal.
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Among 428 older autopsied persons (mean age at death = 91 years, 70% women) considered for anti-amyloid treatment eligibility assessment, 58% had MCI and 42% had mild-stage Alzheimer dementia.
Why it matters
Among 428 autopsied older people considered for anti-amyloid treatment eligibility, several coexisting pathologies such as tangles and arteriolosclerosis were linked to faster cognitive decline. This suggests that even in people eligible for anti-amyloid therapies, other pathologies may still drive decline, but it does not test a treatment, cure or prevention.
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= 0.205; p = 0.651); and between typical (21%) and atypical (11%) subgroups (Fisher's test, p = 0.184).
Why it matters
This study found that a developmental variant could favor early-onset AD/FTD, with symptom onset occurring 8.0 years earlier, but it may not affect susceptibility to typical and atypical variants. The underlying processes require future investigation, so no treatment or prevention is available.
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46/100
Traditional diagnostic methods for Alzheimer's disease often suffer from low accuracy and lengthy processing times, delaying crucial interventions and patient care.
Why it matters
This study compared several deep learning models for classifying Alzheimer's disease from MRI images and found InceptionResNetV2 achieved the highest performance. It is a technical classification study and does not test any treatment, cure, or prevention.
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We analyzed data from 1,542 participants (mean age = 72.2 years, SD = 7.2; 50.8% female; mean education = 16.3 years, SD = 2.6) and found that APOE4 was associated with steeper declines in episodic memory as a function of Aβ duration.
Why it matters
Among people with amyloid buildup, APOE4 carriers, especially those with two copies, showed steeper declines in episodic memory, while other cognitive domains showed no consistent differences. The authors call for future research into whether these differences come from distinct pathologic mechanisms in APOE4 carriers.
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Serum beta-synuclein level was progressively increased in the AD continuum across the preclinical, MCI and dementia stages compared with controls and was correlated with serum pTau181 (r=0.710), NfL (r=0.494) and GFAP concentrations (r=0.621, p<0.001 for all).
Why it matters
Blood levels of beta-synuclein rose step by step across the stages of Alzheimer's disease and distinguished Alzheimer's from controls with high accuracy. This is a promising biomarker for Alzheimer's-related damage to brain connections, but it is not yet a treatment or a cure.
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Alzheimer disease (AD) is a progressive neurodegenerative disease marked by the accumulation of extracellular β-amyloid (Aβ) plaques and intracellular neurofibrillary tangles containing tau protein.
Why it matters
This review notes that many clinical trials targeting amyloid-beta in later disease stages showed limited success in reversing cognitive decline, possibly because treatment started too late. It suggests anti-amyloid-beta approaches may work better when given early, before neuronal damage, while cautioning that amyloid-beta also has normal brain functions that could be disrupted.
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Poor subjective sleep quality is linked to reduced brain volume and cortical thickness (CTh), but associations with objective sleep measures, particularly regarding sex and AD pathology, remain unclear.
Why it matters
This study examined associations between objective sleep measures and brain structure in cognitively unimpaired adults, and how these relate to sex and Alzheimer's biomarkers. It is an observational study and does not test whether improving sleep prevents Alzheimer's disease.
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This paper introduces a novel convolutional neural network model with an attention mechanism to advance Alzheimer disease (AD) classification using Magnetic Resonance Imaging (MRI).
Why it matters
This study introduces a neural network with an attention mechanism for classifying Alzheimer's disease from MRI scans and reports improved diagnostic accuracy. It is a technical classification study and does not test any treatment, cure, or prevention.
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T2DM is one of the strong risk factors of ADRD but genetic T2DM effect does not contribute to ADRD risk.
Why it matters
In a UK Biobank analysis, people with type 2 diabetes had a higher risk of Alzheimer's disease and related dementia than those without, across most subgroups. This links type 2 diabetes to dementia risk but does not show that treating diabetes prevents dementia.
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According to the analysis of the GBD database in 2021, the deaths, DALYs, incidence, and prevalence of ADOD increased by 297.34 %, 249.54 %, 244.73 %, and 250.44 % in Asia from 1990 to 2021.
Why it matters
This analysis of Global Burden of Disease data found large increases in deaths, disability-adjusted life years, incidence, and prevalence of Alzheimer's disease and other dementias in Asia from 1990 to 2021, with high fasting blood glucose the top risk factor. It projects a continued upward trend and calls for intervention measures targeting risk factors.
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Among 635 AD patients without LB, 62 (9.7%) presented parkinsonism, which correlated with reduced nigral neuron density (p < 0.01).
Why it matters
Among 635 Alzheimer's disease patients without Lewy bodies, about one in ten had parkinsonism, which correlated with reduced nigral neuron density and with TDP-43 pathology rather than tau burden. The authors state that recognising parkinsonism in Alzheimer's disease without Lewy bodies is important for appropriate therapy, but no treatment, cure or prevention is tested here.
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BackgroundA novel neuroimaging signature of regional cortical thickness on brain MRI recently showed high potential for Alzheimer's disease and related dementias (ADRD) risk stratification in the community.
Why it matters
This study tried to replicate a novel neuroimaging signature for dementia risk in the Rotterdam Study and found it performed worse than other markers for all-cause dementia, with hippocampal volume showing the strongest associations. It suggests that this particular signature may not be as useful as hoped for risk stratification in the community.
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After controlling for the level of cognitive impairment, we found a double dissociation between AD clinical phenotype and localization/magnitude of atrophy, characterized by predominant neocortical involvement in EOAD and more focal anterior medial temporal involvement in LOAD.
Why it matters
Early-onset and late-onset Alzheimer's disease showed distinct patterns of cortical atrophy, with widespread neocortical involvement in early-onset and more focal anterior medial temporal involvement in late-onset. The authors say MRI-based atrophy markers may help differentiate the two for diagnosis, prognostication, and treatment.
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Plasma biomarkers are promising tools for the screening and diagnosis of dementia in clinical settings.
Why it matters
Blood levels of certain proteins differed between people with Alzheimer's disease and frontotemporal dementia, and combining two or three markers was needed to tell the two conditions apart well. This is about improving diagnosis through blood tests, not about treating or curing either disease.
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In a heterogeneous autopsy sample, AD and LB pathology both contribute to cholinergic basal forebrain degeneration whereas hippocampus atrophy is more specifically related to AD pathology.
Why it matters
In autopsy-confirmed cases, shrinkage of the posterior basal forebrain was most severe in people with mixed Alzheimer's and Lewy body pathology, while hippocampus shrinkage was mainly linked to Alzheimer's pathology. This helps explain how these two diseases overlap in the brain but does not by itself provide a treatment or cure.
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The DLB group had reduced stride velocity, step length, and stride width variability, as well as increased double support percentage (%DS) and variability in step length, swing time, and step time compared to the AD and CU groups.
Why it matters
This study found that gait differs between Alzheimer's disease and dementia with Lewy bodies, but Aβ burden was not associated with any gait outcomes. It is about gait differences, not about treating, curing or preventing dementia.
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The advancement of disease-modifying treatments (DMTs) for Alzheimer's disease (AD), along with the approval of three amyloid-targeting therapies in the US and several other countries, represents a significant development in the treatment landscape, offering new hope for addressing this once untreatable chronic progressive disease.
Why it matters
This is an expert opinion piece, not a study. International dementia researchers say new amyloid-targeting drugs face practical hurdles: deciding who is eligible, using diagnostic and genetic tests, monitoring side effects, getting primary care and specialists ready, and cost and reimbursement. They call for treatment-use criteria built for Europe, better physician training in reading biomarker results and sharing decisions with patients, and patient registries with unbiased follow-up. It reports no new treatment results.
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46/100
Alzheimer's disease is associated with pre-symptomatic changes in brain morphometry and accumulation of abnormal tau and amyloid-beta pathology.
Why it matters
Using cross-sectional and longitudinal data up to 4 years, this study found similar patterns of brain atrophy progression in people at familial risk of Alzheimer's disease and in Alzheimer's disease itself, with more widespread and severe atrophy in Alzheimer's disease. It describes how atrophy progresses and does not test any 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.
- Clinical epidemiology of Alzheimer's disease: assessing sex and gender differences
- CSF Abeta 42 levels correlate with amyloid-neuropathology in a population-based autopsy study
- Molecular imaging of Alzheimer disease pathology
- Association of Amyloid Positron Emission Tomography With Subsequent Change in Clinical Management Among Medicare Beneficiaries With Mild Cognitive Impairment or Dementia
- Incidence trends and age-period-cohort analysis of Alzheimer’s disease and other dementias in the world and China from 1990 to 2021: analyses based on the Global Burden of Disease Study 2021
- Divergent Cortical Tau Positron Emission Tomography Patterns Among Patients With Preclinical Alzheimer Disease
- Amyloid-Related Imaging Abnormalities: An Update
- The role of blood-based biomarkers in Parkinsonian disorders, Alzheimer's disease and frontotemporal dementia
- CSF tau and β-amyloid as biomarkers for mild cognitive impairment
- Behaviour disturbance and other predictors of carer burden in Alzheimer's disease