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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87 DLB patients (77.5 ± 7.2yo; 34.5 % females) were included.
Why it matters
Among 87 patients with dementia with Lewy bodies, 65.5% had cerebral amyloid angiopathy, but cognitive performance and hippocampal volumes were similar whether or not it was present. The study concludes that cerebral amyloid angiopathy does not affect cognition or hippocampal volume in these patients.
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35/100
Alzheimer’s disease (AD), the leading cause of dementia, is a multifaceted neurodegenerative disorder characterized by amyloid-beta (Aβ) aggregation, tau pathology, and neuroinflammation.
Why it matters
This review describes three monoclonal antibodies—lecanemab, gantenerumab and donanemab—that target amyloid-beta and are reported to reduce amyloid burden and slow cognitive decline, while carrying risks such as amyloid-related imaging abnormalities. It is a summary of these therapies, not new evidence of a cure or prevention.
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In 1906, Alois Alzheimer first described the neuropathological hallmarks of the disease that now bears his name.
Why it matters
In 247 participants, a panel of cerebrospinal fluid biomarkers (t-tau, p-tau181 and Aβ42) distinguished Alzheimer's disease from controls with 94.3% sensitivity and 91.7% specificity, and from non-Alzheimer's dementias with 87.8% sensitivity and 84.2% specificity. The authors support using these biomarker panels for early detection, especially at the mild cognitive impairment stage when treatments may have the greatest potential benefit, but this is a diagnostic study, not a treatment or cure.
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To determine the degree to which patients with early Alzheimer disease (AD) being evaluated for anti-amyloid antibody therapies (AATs) adhere to optimal brain-health/lifestyle recommendations.
Why it matters
This study set out to measure how well patients with early Alzheimer's disease being evaluated for anti-amyloid antibody therapies follow brain-health and lifestyle recommendations. No results on adherence or treatment outcomes are reported in the available text.
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Low income and vulnerability to arterial hypertension were the primary contributors to AD/ADRD disparities, with cerebrovascular diseases and depression as notable secondary predictors.
Why it matters
This study found that low income and vulnerability to hypertension were the primary contributors to Alzheimer's disease and related dementias disparities. It suggests that different intervention strategies are needed, such as socioeconomic improvements for income-related disparities and better hypertension control for hypertension-related disparities.
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35/100
Alzheimer's disease (AD) is a multifactorial disorder associated with neuroinflammation, elevated oxidative stress, lipid alterations as well as amyloid-deposits and the formation of neurofibrillary tangles.
Why it matters
In laboratory lipid studies, ibuprofen raised some lipids that are low in Alzheimer's brain tissue but also raised triglycerides linked to neuroinflammation and lowered plasmalogens, which are already reduced in Alzheimer's brains. This means ibuprofen's effects on brain lipids are mixed, with both potentially helpful and potentially harmful changes, so it cannot be assumed to slow or prevent the disease.
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H]UCB-J was found to be reduced in frontal cortex from patients with AD.
Why it matters
The reduction in SV2A binding was highly significant only in Alzheimer's disease patients not carrying the ApoE ε4 allele, while carriers had levels not different from controls. This is an unexpected association between ApoE4, SV2A, and synapse loss, not a treatment, cure, or prevention.
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Florbetaben (FBB) is a radiopharmaceutical approved by the FDA and EMA in 2014 for the positron emission tomography (PET) imaging of brain amyloid deposition in patients with cognitive impairment who are being evaluated for Alzheimer's disease (AD) or other causes of cognitive decline.
Why it matters
This review describes a decade of experience with florbetaben amyloid PET, which is used to confirm amyloid plaques and monitor responses to amyloid-lowering therapies. It does not test any treatment, cure, or prevention for Alzheimer's disease.
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Alzheimer's disease (AD), the most common form of dementia, is marked by cognitive decline and amyloid-beta (Aβ) plaque deposition in the brain.
Why it matters
In postmortem brain tissue from 75 older adults, plaque-associated microglia in certain layers were linked to worse memory scores. This is a study of brain tissue and cognitive scores, not a treatment or prevention strategy.
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Most branched-chain amino acids, except isoleucine (Ile), are correlated with both mild cognitive impairment (MCI) and AD.
Why it matters
This study investigated whether serum isoleucine levels are associated with mild cognitive impairment and Alzheimer's disease in 700 participants from the Alzheimer's Disease Neuroimaging Initiative database. It reports an association with diagnosis and does not test any treatment, cure or prevention.
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Alzheimer's disease (AD) is a neurodegenerative disease that imposes economic and societal burden.
Why it matters
This paper states that biomarkers played a crucial role in the recent approval of aducanumab and lecanemab as disease-modifying therapies. It analyzed how biomarkers are used as endpoints in Alzheimer's disease trials to support diagnosis, safety monitoring and disease modification.
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Alzheimer´s disease is considered a neurodegenerative disease and is diagnosed by exclusion, while the detection of specific cerebrospinal fluid (CSF) biomarkers, namely amyloid-beta (Aβ) peptides Aβ1-42 (Aß42), phospho-tau (181P; P-tau), and total-tau (T-tau), has been shown to improve diagnostic accuracy.
Why it matters
This study examined how pre-analytical factors affect Elecsys immunoassay measurements of CSF Aβ42, P-tau and T-tau in 29 patients without an Alzheimer's disease diagnosis, finding stability except with freezing at -80 °C. It concerns laboratory handling of biomarker samples, not treating, curing or preventing the disease.
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AD mortality rates significantly increased over time.
Why it matters
Alzheimer's disease mortality rates among American Indian and Alaska Native people increased over time, and more deprived counties had 34% higher mortality while nonmetro counties had 20% lower mortality. The authors say the findings can help prioritize areas needing more resources for Alzheimer's disease care, education, or outreach, but this does not identify a treatment, cure, or prevention.
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Amyloid-related imaging abnormalities with edema (ARIA-E) have been reported in patients with early Alzheimer disease treated with aducanumab.
Why it matters
This modelling study used data from two phase 3 trials to describe how aducanumab serum exposure affects the risk of amyloid-related imaging abnormalities with edema (ARIA-E) and their resolution. It found that ARIA-E incidence depends on both dose and apolipoprotein E4 carrier status, which is a safety finding rather than evidence of clinical benefit.
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Aducanumab was approved by the Food and Drug Administration (FDA) in June 2021 to treat Alzheimer disease (AD).
Why it matters
Aducanumab's accelerated approval was based on a surrogate end point, with evidence of clinical effectiveness still pending a postapproval trial by the sponsor Biogen. The paper states that the drug's role in treating Alzheimer's disease remains uncertain.
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Phosphorylated tau (pTau), total tau (tTau), and β-amyloid (Aβ) are established cerebrospinal fluid (CSF) biomarkers used to help diagnose Alzheimer disease.
Why it matters
This study compared different polypropylene collection tubes to see how much amyloid is lost by sticking to tube walls, since low measured levels could lead to a false Alzheimer's diagnosis. It is about standardizing how cerebrospinal fluid samples are handled, not about treating, curing or preventing the disease.
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Cerebrospinal fluid (CSF) amyloid-beta (Aβ) 42/40 ratio, threonine-181-phosphorylated-tau (p-tau), and total-tau (t-tau) represent core biomarkers of Alzheimer disease (AD).
Why it matters
This work checked whether Alzheimer's biomarker values measured in fresh spinal fluid samples match those measured in frozen samples. It is a laboratory methods question about testing, with no bearing on treating or curing the disease.
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35/100
Areas within the Appalachian region may have a greater burden of under diagnosed Alzheimer's disease and related disorders (ADRD).
Why it matters
This study found that Alzheimer's and related disorders prevalence among Medicare beneficiaries in Ohio differed by Appalachian residence and rural status, with rural Appalachian counties showing higher prevalence after adjustment. It describes geographic patterns of prevalence, not treatment or prevention.
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Alzheimer's disease (AD) is a multifactorial disorder that involves several different mechanisms.
Why it matters
This study reports that certain symptoms such as hallucinations, paranoia, rigidity, and tremors may help predict which subtype of Alzheimer's disease a person has. It is about classifying patients, not about treating or curing the disease.
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When evaluating the 'bleeding load' with 7.0-T T₂*-weighted MRI in post-mortem brain sections of patients with dementia and vascular risk factors, only quantification of small cerebral bleeds in the cortico-subcortical regions is reliable.
Why it matters
In post-mortem brain sections, 7.0-T T2*-weighted MRI reliably detected small cerebral bleeds only in cortico-subcortical regions, with overestimation in the striatum and missed bleeds in deep white matter. This is a validation of an imaging method for measuring bleeding load, not a treatment, cure or prevention for Alzheimer's disease.
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In common forms of Alzheimer disease (AD), anterograde memory impairment is the first deficit to occur.
Why it matters
This study asked whether the clinical profile of early-onset Alzheimer's disease, memory versus non-memory onset, affects cerebrospinal fluid levels of total tau, phosphorylated tau and amyloid-beta 42. It is a biomarker comparison, so it does not provide a treatment, cure or prevention.
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The progressive nature of neurodegeneration suggests an age-dependent process that ultimately leads to synaptic failure and neuronal damage in cortical areas of the brain critical for memory and higher mental functions.
Why it matters
This review states that evidence supports an imbalance between production and removal of beta-amyloid as central to Alzheimer disease, and that understanding of how beta-amyloid forms and damages neurons is being turned into new treatment approaches. It notes that without specific biologic markers, direct examination of brain tissue is still the only definitive way to diagnose Alzheimer disease and other dementias.
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Neurofibrillary degeneration (ND) is both a pivotal and a primary lesion of Alzheimer disease (AD) and related tauopathies.
Why it matters
This paper reviews the role of abnormally phosphorylated tau and neurofibrillary degeneration in Alzheimer's disease and related tauopathies. It discusses the idea of blocking this process as a possible approach, but no treatment is tested here.
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Tau protein is a microtubule-associated protein located in neuronal axons, which has been used in various configurations as a diagnostic marker of degenerative changes in the CNS.
Why it matters
This study evaluated cerebrospinal fluid total tau to tell Alzheimer-type dementia apart from vascular dementia and controls. It is a diagnostic comparison, so it does not provide a treatment, cure or prevention.
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Immunocytochemistry, Western blotting, and RT-PCR were used to identify the isoforms of laminin expressed in the Alzheimer disease, but not in normal human brain tissue.
Why it matters
In Alzheimer's disease brain tissue, alpha 1 and gamma 1 laminins were over-expressed in reactive astrocytes and found as punctate deposits in senile plaques, unlike in normal brain tissue. This describes an association between these laminins and Alzheimer's disease pathology, but the study does not show whether they cause the disease or could be a treatment target.
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.
- Rare coding mutations identified by sequencing of Alzheimer disease genome-wide association studies loci
- Rate of conversion from prodromal Alzheimer's disease to Alzheimer's dementia: a systematic review of the literature
- Periodontitis and Cognitive Decline in Alzheimer's Disease
- Cerebral perfusion in the predementia stages of Alzheimer's disease
- Synapse loss in frontal cortex biopsies in Alzheimer's disease: Correlation with cognitive severity
- Review of Artificial Intelligence for Clinical Use in Alzheimer's Disease and Related Dementias
- Individual analysis of EEG frequency and band power in mild Alzheimer's disease
- Triazole Hybrids for Alzheimer's Disease: Multitarget Potential and SAR Insights
- Associations of Stages of Objective Memory Impairment With Amyloid PET and Structural MRI: The A4 Study
- Lower cerebral blood flow is associated with faster cognitive decline in Alzheimer's disease