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 5,413 studies, highest score first: BibTeX (.bib) · RIS (.ris)
Highest usefulness score first. Studies without a score come last.
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This widely cited review examined the long-running debate over whether amyloid or tau comes first in Alzheimer's disease.
Why it matters
The authors argue amyloid buildup is the initial trigger starting the disease 20-30 years before symptoms, while tau emerges later and is what drives neurodegeneration and cognitive decline. This frames tau as the closer target for slowing decline, but it is a review of existing evidence rather than a new treatment result.
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Treatment outcomes in the DIADS-2 trial were not significantly influenced by genetic variation at the loci that were assessed.
Why it matters
This analysis of data from a trial that found no significant effect of sertraline on depression in Alzheimer's disease found no significant link between any of the four genetic variants studied and treatment outcomes. It does not show a way to treat, cure or prevent Alzheimer's disease.
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Patients at late stage Parkinson's disease (PD) develop several motor and nonmotor complications, which dramatically impair their quality of life.
Why it matters
This review discusses treatment of advanced Parkinson's disease, including dementia as one complication, and emphasizes balancing pharmacological benefits and side effects. It is about Parkinson's disease management, not about treating, curing or preventing Alzheimer's disease.
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Alzheimer's disease (AD) is the leading cause of dementia.
Why it matters
This study examined whether cerebrospinal fluid beta-amyloid 1-42 and total tau could help diagnose Alzheimer's disease in Tunisian participants. It is a diagnostic biomarker study, so it does not show any treatment, cure or prevention.
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To investigate the mRNA expression of the dendritic spine protein drebrin in Alzheimer's disease (AD), we performed post-mortem in situ hybridization studies in brain sections from 20 AD patients and 21 controls.
Why it matters
Using post-mortem brain tissue from 20 Alzheimer's disease patients and 21 controls, this study found decreased drebrin mRNA expression that correlated with tau pathology. It is a tissue study describing disease-related changes, not a treatment, cure, or prevention for Alzheimer's disease.
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There is a substantial body of literature dealing with predictors of dementia in patients with MCI.
Why it matters
This review describes predictors that may help identify which people with mild cognitive impairment will go on to develop Alzheimer's dementia. It reports that APOE epsilon 4 raises conversion risk but with low sensitivity, and that CSF markers such as beta-amyloid 42 and tau are still being developed.
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It is estimated that approximately 40,000 people in Denmark suffer from Alzheimer's disease (AD), a neurodegenerative dementia.
Why it matters
This paper discusses that Alzheimer's disease is difficult to diagnose early and that a definite diagnosis is only possible post-mortem, while reviewing biomarkers for distinguishing it from normal aging and other dementias. It concerns diagnosis and does not report any treatment, cure, or prevention.
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Aging of the brain has been demonstrated to be the main risk factor for late-onset sporadic AD what is in contrast to early-onset familial AD in which mutations predominate the pathology.
Why it matters
This review proposes that age-related changes in neuronal insulin/insulin receptor signalling contribute to late-onset sporadic Alzheimer's disease. It is a hypothesis based on prior findings and does not report a treatment or prevention tested in people.
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Deregulation of amyloid precursor protein (APP) processing with increased production of amyloid beta-peptide (Abeta) is considered to be a key pathogenic event in Alzheimer's disease (AD).
Why it matters
Blood levels of Abeta42 and Abeta40 were measured in people with Alzheimer's before and during treatment with tacrine, an acetylcholinesterase inhibitor. Tacrine had no significant overall effect at 2 or 6 weeks; higher drug levels were tied to lower amyloid at 2 weeks, but that link was gone by 6 weeks. The authors suggest compensatory mechanisms may set in and that no long-term effect on key Alzheimer's features is to be expected from this type of drug.
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We tested whether familial aggregation of Down syndrome and Alzheimer's disease (AD) is present for trisomies of other autosomes.
Why it matters
Rates of Alzheimer-like dementia were not increased in parents of women who had trisomic pregnancy losses involving autosomes other than chromosome 21. The authors say their data do not support an association between Alzheimer's disease and trisomy of all autosomal chromosomes, and raise the possibility that any familial link is specific to trisomy 21.
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Cross-sectional and longitudinal analyses were used to compare age-related changes in adaptive functioning in institutionalized adults with and without Down syndrome.
Why it matters
This cross-sectional and longitudinal study found declines in self-help and communication skills in some adults with Down syndrome older than 40, and presented one case with confirmed Alzheimer pathology at postmortem. It describes age-related changes, not any treatment, cure or prevention.
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It is hypothesized that Alzheimer's disease is a human phylogenetic disease which has a common multifactorial pathogenesis in sporadic and familial cases and in Down syndrome, related to a genomic character function G(x).
Why it matters
This paper hypothesizes that Alzheimer disease is a human phylogenetic disease with a shared cause in sporadic, familial, and Down syndrome cases. It is a hypothesis only and offers no treatment, cure, or prevention.
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The vascular and parenchymal amyloid deposits in Alzheimer disease (AD), normal aging and Down syndrome are mainly composed of a 4 kDa polypeptide (A4), which derives from a larger precursor protein (APP).
Why it matters
This laboratory study describes two forms of the amyloid precursor protein in cultured cells. It does not test any treatment or prevention for Alzheimer disease.
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37/100
Progressive electroencephalographic disorganization and decreased voltage amplitude in the late components of the averaged visual evoked potentials were recorded in the last two years of life of a patient with Down disease and Alzheimer degeneration.
Why it matters
In one patient with Down syndrome and Alzheimer degeneration, progressive EEG disorganization and decreased visual evoked potential amplitude were recorded in the last two years of life and interpreted alongside histopathologic findings. This is a single-case observational study and does not test any treatment.
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A doença de Alzheimer (DA) é uma enfermidade neurodegenerativa progressiva cuja fisiopatologia envolve, entre outros mecanismos, o acúmulo cerebral de β-amiloide, associado a alterações da proteína tau, sua hiperfosforilação e formação de emaranhados neurofibrilares, contribuindo para a disfunção sináptica e a perda neuronal.
Why it matters
This review of 26 studies found that blood levels of p-tau217 were associated with amyloid deposition and tau pathology and with identifying preclinical changes and stratifying patients. The authors present p-tau217 as a promising blood biomarker for early identification of Alzheimer's disease.
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Type 2 diabetes (T2D) and dementia frequently co-occur, yet the biological mechanisms underlying this comorbidity remain incompletely understood.
Why it matters
This genetic study identified shared genetic signals between type 2 diabetes and three forms of neurodegenerative dementia, including the APOE locus common to all dementia subtypes. The findings reveal systemic metabolic-neurodegenerative trade-offs and provide a framework for understanding comorbidity, but do not directly lead to a treatment or cure.
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Recent advances in Blood-Based Biomarkers (BBMs) are transforming the diagnostic landscape of Alzheimer Disease (AD), with plasma p-tau217 emerging as a highly accurate and scalable diagnostic marker of AD pathology.
Why it matters
Plasma p-tau217 showed consistently strong diagnostic performance for detecting amyloid pathology across multiple platforms, and its performance was largely preserved in older adults with multimorbidity, kidney disease, polypharmacy and frailty. Current evidence and guidelines support its use only in symptomatic older adults, so this is a diagnostic advance, not a treatment or cure.
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36/100
Blood-based biomarkers are increasingly used to triage patients for amyloid confirmation, yet performance is often reported versus a single comparator despite discordance between amyloid PET and CSF.
Why it matters
This study used statistical modeling to estimate the probability of amyloid positivity from blood, spinal fluid, and PET scan results, finding that discordant results between PET and spinal fluid gave intermediate probabilities. It is a diagnostic interpretation study and does not test any treatment, cure, or prevention.
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36/100
Objetivo:Analisar criticamente o potencial dos exossomos sanguíneos associados a marcadores inflamatórios e ferramentas nanotecnológicas como biomarcadores hematológicos no diagnóstico precoce da Doença de Alzheimer (DA), enfatizando aplicações translacionais.
Why it matters
This review of studies from the last 10 years reports that exosomes in the blood carry Alzheimer's-related proteins and microRNAs, and that inflammatory markers like IL-1β, IL-6, IL-8 and TNF-α are consistently linked to worsening neurodegeneration. The authors suggest combining hematology, molecular neuroscience and nanotechnology could one day allow early diagnosis and monitoring through a blood test, but this is a review of existing evidence, not a new treatment or cure.
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Alzheimer's disease (AD) affects ~55 million people globally and is projected to rise steeply with population ageing.
Why it matters
This review summarizes evidence linking oral bacteria and periodontal disease to faster cognitive decline and higher dementia risk, with proposed pathways including neuroinflammation, blood-brain barrier dysfunction, and microbial components in neural tissue. It is a narrative review of possible contributors to Alzheimer's disease, not a trial showing that treating oral infection prevents or cures it.
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-glycans found at the N304 site of lecanemab of the heavy chain.
Why it matters
This laboratory analysis characterised lecanemab's structure and modifications by mass spectrometry. It provides data as a resource for identifying critical quality attributes of lecanemab, not evidence that the drug treats, cures or prevents Alzheimer disease.
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Event-related potentials (ERPs), particularly the P300 component, provide a noninvasive, cost-effective approach to probing neural dysfunction in Alzheimer's disease (AD) and mild cognitive impairment (MCI).
Why it matters
This review found that P300 latency is most consistently prolonged in Alzheimer's disease, especially in auditory oddball tasks, while amplitude reductions were less reliable. It does not test any treatment or cure, so it only suggests that EEG-based P300 measures may help distinguish these groups if methods are standardized.
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Accurate and reproducible electroencephalography (EEG)-based classification of dementia remains a key challenge in computational neurodiagnostics.
Why it matters
This review found that reported accuracy for dementia classification drops when stricter validation methods are used, from 90.81% to 82.11% for Alzheimer's versus controls. It is a methodological analysis of existing studies, so it does not offer a treatment, cure or prevention.
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The Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND) diet has emerged as a promising dietary pattern associated with reduced Alzheimer's disease (AD) risk, supported by growing evidence that both diet and the gut microbiota are modifiable contributors to disease development and progression.
Why it matters
This review discusses how the MIND diet may reduce Alzheimer's disease risk and proposes the gut microbiota as a possible link between diet and brain function. It notes that direct evidence on the MIND diet's effects on gut bacteria is limited, so the mechanism remains unproven.
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Here the current and emerging roles of brain positron emission tomography (PET) in Alzheimer's disease (AD) in the era of anti-amyloid-β antibody therapy, with a focus on clinical applications, methodological considerations, and future perspectives were reviewed.
Why it matters
This review describes how amyloid PET is essential for confirming eligibility for anti-amyloid therapies, tau PET reflects neurofibrillary pathology and disease severity, and FDG PET supports differential diagnosis. It is about imaging's role in diagnosis and monitoring, not a treatment or cure.
From across this topic
10 of the 5,374 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.
- Structural magnetic resonance imaging for the early diagnosis of dementia due to Alzheimer's disease in people with mild cognitive impairment
- Statin Initiation and Risk of Incident Alzheimer Disease and Cognitive Decline in Genetically Susceptible Older Adults
- TYROBP genetic variants in early-onset Alzheimer's disease
- Delusions and hallucinations in Alzheimer's disease: prevalence and clinical correlates
- Evaluation of a panel of plasma biomarkers for Alzheimer's disease in a diverse research cohort
- [Diagnosing Alzheimer Dementia in People with Down Syndrome in Accordance with ICD, DSM V and A/T/N System]
- Plasma biomarkers identify brain ATN abnormalities in a dementia-free population-based cohort
- Shared genetic architecture between brain iron deposition and Alzheimer's disease
- The efficacy of Ginkgo biloba on cognitive function in Alzheimer disease
- Regional distribution of white matter hyperintensities in vascular dementia, Alzheimer's disease and healthy aging