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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Alzheimer disease (AD) is accompanied by a marked loss of acetylcholinesterase (AChE) activity associated with cortical cholinergic axons and cholinoceptive neurons.
Why it matters
This study describes loss of acetylcholinesterase activity in Alzheimer's cortex alongside new cholinesterase activity associated with plaques, tangles and amyloid angiopathy, with different enzymatic properties. It is a description of pathology and reports no treatment, cure or prevention.
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Microtubule associated protein tau is abnormally phosphorylated in Alzheimer disease (AD) brain.
Why it matters
This study measured levels of normal and abnormally phosphorylated tau in different parts of brain tissue from people who had died with Alzheimer disease and from controls. It is a postmortem tissue analysis and does not test any treatment, cure, or prevention.
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The Alzheimer amyloid protein precursor (APP) has previously been localized to human chromosome 21q11.2-q21.
Why it matters
This study narrowed the location of the amyloid precursor protein gene on chromosome 21 and excluded it from the region causing classic Down syndrome features. It is basic mapping and does not test any treatment.
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Recent studies have indicated a normal gene dose for the amyloid precursor protein (APP) in Alzheimer's disease (AD).
Why it matters
In brain tissue from six people with Alzheimer's disease, levels of messenger RNA for amyloid precursor protein and for two cytoskeletal proteins were lower than in six control samples, while the message for GFAP showed no loss. This supports a general loss of neuronal RNA messages in advanced disease, but the study could not rule out higher amyloid precursor protein message in small groups of neurons or in earlier stages.
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The presence of abundant intraneuronal amyloid in the form of neurofibrillary tangles (NFT) in the brains of Guamanian parkinsonism-dementia patients and the absence of extraneuronal amyloid in the form of vascular amyloid deposits or senile plaques permit the purification of NFT without contamination with extraneuronal amyloid.
Why it matters
The amyloid protein in neurofibrillary tangles from Guamanian parkinsonism-dementia patients was found to have the same amino acid sequence as amyloid in Alzheimer's disease and Down syndrome brains. This laboratory finding suggests a common pathogenesis but does not provide a treatment or cure.
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Anti-amyloid monoclonal antibodies (lecanemab and donanemab) represent the first disease-modifying therapies for early symptomatic Alzheimer's disease (AD)- Italy's National Health Service (SSN) must determine whether to include these therapies within Essential Levels of Care (LEA), requiring reimbursement across all regions.
Why it matters
This scenario analysis estimated that about 42,000 patients in Italy could be eligible for anti-amyloid monoclonal antibodies, and that a moderate uptake scenario reaching 14,100 patients over three years would cost €557.3 million, about 0.4% of the annual national health service budget. It is a budget and feasibility modelling exercise, not evidence that these therapies cure or prevent Alzheimer's disease.
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Alzheimer's Disease (AD), the most common form of dementia, is pathologically defined by extracellular beta-amyloid (Aβ) plaques and intraneuronal neurofibrillary tangles (NFTs), accompanied by chronic neuroinflammation.
Why it matters
This review of single-cell and spatial transcriptomics describes state changes in microglia and astrocytes and regional differences around plaques in Alzheimer's disease. It is a review of research methods and findings, not a treatment or cure, and it does not report a therapy tested in patients.
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Alzheimer's disease (AD) is the leading cause of dementia worldwide and represents a growing public health challenge in aging societies.
Why it matters
This review describes nanoparticle-based drug delivery systems designed to carry Alzheimer's therapies across the blood-brain barrier, which currently blocks most treatments from reaching the brain. It notes that efficient brain penetration and clinical translation remain major challenges, so no treatment is yet proven.
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In the AD and non-AD group, OEF showed negative associations with WMH in DGM and positive associations with MoCA in DGM and CGM.
Why it matters
This study found that a measure of oxygen use in brain tissue related to cognitive scores and to small-vessel changes in people with Alzheimer's and non-Alzheimer's dementias. The authors suggest this measure may help tell the two types of dementia apart, but the study did not test any treatment.
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Key recommendations emphasize that tissue biopsies remain essential for amyloidosis diagnosis and typing.
Why it matters
These Belgian recommendations address tissue diagnosis of amyloidosis, emphasizing that biopsies remain essential and describing staining, subtyping and centralized analysis. They concern diagnosis of amyloidosis generally and do not present a treatment, cure or prevention for Alzheimer's disease.
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38/100
Participants’ motivations for testing and long-term adaptation to the results were strongly shaped by cognitive concerns and personal experiences of dementia in relatives.
Why it matters
Three years after learning their amyloid PET results, people with subjective cognitive decline had adjusted to living with the information without ongoing psychological harm and valued testing. This addresses the experience of disclosure rather than treating, curing or preventing the disease.
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Alzheimer's disease (AD) is the most common cause of dementia, affecting 55 million people worldwide.
Why it matters
This review covers progress in machine learning-assisted biosensors for detecting Alzheimer's disease biomarkers such as microRNAs, amyloid peptides, Tau protein, and neurofilament light chains in bodily fluids. It is about early detection technology, not about treating, curing, or preventing the disease.
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Alzheimer's disease (AD) is a neurodegenerative disease characterized by progressive accumulation of toxic amyloid species.
Why it matters
This paper discusses anti-amyloid therapies that have shown statistically significant group-level slowing of disease progression in early symptomatic Alzheimer's disease in pivotal trials. It notes a lack of data on Asian populations and highlights the need to translate trial outcomes into benefits that are meaningful to patients and caregivers.
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Across AD, ALS, and FTD, a convergent multimorbidity architecture centered on a shared metabolic and immune core was identified, accompanied by prominent neurobehavioral processes and intermediate systems including gastrointestinal, endocrine, hematological, hepatic, and sensory pathways.
Why it matters
This computational study identifies a shared metabolic and immune core across Alzheimer's disease, ALS and frontotemporal dementia, providing a hypothesis-generating foundation for biomarker discovery and cross-disease therapeutic exploration. It is a computational analysis only and does not test any treatment, cure or prevention.
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Socioeconomic disadvantage (SED) has been associated with poorer brain health, yet its underlying pathology remains incompletely understood.
Why it matters
In 1,110 participants, higher neighborhood socioeconomic deprivation was associated with lower MMSE scores and greater amyloid burden among cognitively unimpaired participants. This links social disadvantage to early AD-related pathology but does not test any treatment, cure, or prevention.
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To evaluate the possible causality between Alzheimer disease (AD) and delirium, a two-sample Mendelian randomization (MR) method and gene colocalization strategy were employed.
Why it matters
Mendelian randomization indicated a causal influence of Alzheimer's disease on delirium occurrence, with shared genetic loci NECTIN2 and TOMM40 as potential mediators. No evidence of reverse causality was identified, highlighting potential preventive targets for delirium in Alzheimer's patients.
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Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia worldwide and is associated with substantial morbidity and mortality, including stroke, systemic embolism, heart failure, and dementia.
Why it matters
This review describes how AI could help detect atrial fibrillation earlier and guide its treatment, and it notes that atrial fibrillation is linked to dementia among other conditions. It does not test whether treating atrial fibrillation with AI-guided care prevents or cures Alzheimer's disease.
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PRS correlated positively with log-NFL (r = 0.31, p = 0.004) and inversely with N3 duration (r = −0.26, p = 0.017).
Why it matters
In midlife, higher polygenic risk for Alzheimer's correlated with higher plasma neurofilament light chain, and this association was stronger at shorter N3 sleep duration. The authors state these cross-sectional findings do not establish causality or Alzheimer-specific pathology.
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Alzheimer's disease (AD) and related dementias (ADRD) are neurodegenerative conditions that cause gradual deterioration of cognition, memory and language in the elderly.
Why it matters
This paper notes that African American and Hispanic populations have a higher prevalence of Alzheimer's and related dementias, with risk approaching twice that of White individuals, and that epigenomic research may help explain these disparities. It is a review of the field and does not test any treatment, cure, or prevention.
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The AD PRS was associated with AD in the ADSP sample, with odds ratios per standard deviation ranging from 1.14 to 1.52 across ancestry groups and robust validation in independent cohorts (Figure 1).
Why it matters
A polygenic risk score was associated with Alzheimer disease across ancestry groups, and the association was stronger in people with vascular conditions. Among women with high genetic risk, ever-use of hormone replacement therapy was linked to better memory trajectories, especially when started within five years of menopause, but this is an observational finding, not proof of a treatment effect.
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Alzheimer Disease (AD) is a highly polygenic dementia that presents with relatively earlier onset (≤65yo; EOAD) in about 5% of cases.
Why it matters
Eight novel genome-wide significant loci for early-onset Alzheimer's disease were identified, with four functional genes involved in microglia activation, glutamate production, and signaling pathways. Early-onset Alzheimer's shares many genes with late-onset but harbors unique genetic contributors.
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The MDC used a combination of CSF tests, blood tests, and amyloid PET scans to scale up AD biomarker testing over the past three years.
Why it matters
This study describes how a specialty memory clinic used different Alzheimer's disease biomarker tests over time and the rates of biomarker positivity by sex and racial group, based on 970 patients tested between June 2021 and December 2024. It is a description of testing patterns in one clinic and does not test any treatment, cure or prevention.
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The Boston v2.0 criteria have low accuracy in patients with AD dementia.
Why it matters
In 63 autopsy-confirmed dementia cases, 60.3% did not meet the Boston v2.0 criteria for cerebral amyloid angiopathy, and 45% of those had moderate or severe CAA. This indicates the MRI-based criteria missed CAA in many patients, which matters for assessing ARIA risk, but the study tests diagnosis, not treatment or cure.
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Compared to CN, we identified 32 differential metabolites in AD and 49 in MCI serum.
Why it matters
This study identified panels of 10 metabolites in Alzheimer's disease and 13 in mild cognitive impairment that distinguished these groups from cognitively normal controls with high accuracy. These are blood-based metabolite signatures for classification, not a treatment or cure.
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This study replicated the associations of SORL1, CR1, ADAM17, RASGEF1C, SPI1 , and ADAMTS1 with AD risk and protection are found in Cuban Americans.
Why it matters
In 239 Cuban American individuals, this study replicated SORL1, CR1, ADAM17 and RASGEF1C as risk loci for Alzheimer's disease and found SPI1 and ADAMTS1 as protective loci, with APOE4 also significantly associated. These are genetic association findings that may inform risk understanding but do not treat or prevent 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.
- Atherosclerosis, apolipoprotein E, and prevalence of dementia and Alzheimer's disease in the Rotterdam Study
- Benfotiamine and Cognitive Decline in Alzheimer's Disease: Results of a Randomized Placebo-Controlled Phase IIa Clinical Trial
- MiR-124 acts as a target for Alzheimer's disease by regulating BACE1
- Cerebral amyloid angiopathy burden associated with leukoaraiosis: a positron emission tomography/magnetic resonance imaging study
- Amyloid age and tau PET timeline to symptomatic Alzheimer’s disease in Down syndrome
- Consensus Recommendations for the Postmortem Diagnosis of Alzheimer’s Disease
- Imaging of amyloid beta in Alzheimer's disease with 18F-BAY94-9172, a novel PET tracer: proof of mechanism
- Decreased expression and activity of neprilysin in Alzheimer disease are associated with cerebral amyloid angiopathy
- The APOE-epsilon4 allele and the risk of Alzheimer disease among African Americans, whites, and Hispanics
- White matter lesions on magnetic resonance imaging in dementia with Lewy bodies, Alzheimer's disease, vascular dementia, and normal aging