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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Disclosure (N = 194) and non-disclosure (N = 180) groups did not differ on IGT-AD (mean disclosure-non-disclosure difference [MD] at 6 weeks: -1.5, p = 0.14; 9 months: -1.2, p = 0.35; 15 months: -2.0, p = 0.07), IES-R (MD at 6 weeks: 0.00, p = 0.98; 9 months: 0.01, p = 0.84; 15 months: 0.03, p = 0.64), or change in secondary outcomes.
Why it matters
In a Latino cohort, APOE genotype disclosure did not have clinically significant adverse psychological effects compared to non-disclosure. This addresses an important evidence gap regarding the safety of genetic risk disclosure.
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White matter hyperintensities (WMHs) are neuroimaging markers widely interpreted as caused by cerebral small vessel disease, yet emerging evidence suggests that a subset may have a neurodegenerative etiology.
Why it matters
Using MRI in a large cohort, the researchers identified a pattern of white matter hyperintensities with a posterior predominance that was linked to dementia and Alzheimer's disease and appeared to reflect fibre degeneration rather than only vessel disease. This may help separate vascular from neurodegenerative causes of these lesions, but it does not test any treatment.
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's ≥ 0.75). Both markers identified Braak stage V-VI levels with similarly high performance (entorhinal SUVR, area under the curve [AUC] = 0.92 [95% CI 0.91-0.93]; temporal meta-ROI SUVR, AUC = 0.91 [95% CI 0.90-0.92]; plasma p-tau217, AUC = 0.90 [95% CI 0.89-0.91]), but PET outperformed plasma p-tau217 in identifying high/intermediate ADNCs (entorhinal ROI, AUC = 0.94 [95% CI 0.94-0.95]; temporal meta-ROI AUC = 0.94 [95% CI 0.94-0.95]; plasma p-tau217, AUC = 0.89 [95% CI 0.88-0.90]).
Why it matters
Both flortaucipir-PET and plasma p-tau217 identified advanced Braak stages with similarly high performance, but PET was better at identifying high or intermediate Alzheimer's neuropathologic change. Both markers were specific for primary Alzheimer's diagnosis but had limited sensitivity for early tau co-pathology in non-Alzheimer's diagnoses.
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58/100
A total of 1,345 individuals were included.
Why it matters
In this study of 1,345 people, cerebrospinal fluid GFAP did not show clinically relevant diagnostic or prognostic value in dementia. Further studies are needed to clarify its role in Parkinson's disease dementia.
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The APOE ε4 genetic variant is the strongest genetic risk factor for late-onset Alzheimer's disease (AD) and is increasingly being implicated in other neurodegenerative diseases.
Why it matters
This study found that APOE ε4 carriers share immune-related proteomic changes across several neurodegenerative diseases, suggesting APOE ε4 confers a systemic biological vulnerability that is necessary but not sufficient for neurodegeneration. It is a biomarker and mechanism study and does not test any treatment, cure or prevention.
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58/100
Of 413 477 All of Us participants, 2038 were eligible.
Why it matters
In people with atrial fibrillation taking apixaban, carrying APOE ε4 was linked to about a threefold higher risk of intracranial hemorrhage. The authors say further research is needed to see whether this association is mediated by cerebral amyloid angiopathy and whether APOE ε4 information improves decisions about anticoagulation therapy.
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Late-life depression (LLD) has been linked to increased likelihood of dementia, although mechanisms responsible for this association remain largely unknown.
Why it matters
Several plasma inflammatory markers were higher in older people with late-life depression than in controls, but among clinical features only poor response to treatment significantly predicted progression to dementia within three years. The findings suggest inflammation may be relevant to late-life depression, but they do not show that treating inflammation prevents dementia.
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The role of microglia in the amyloid cascade of Alzheimer's disease (AD) is debated due to conflicting findings.
Why it matters
Using genetic and pharmacological approaches, this study found that depleting microglia before amyloid-β plaque deposition reduced plaque numbers and neuritic dystrophy, while transplanting human microglia restored plaque formation. It also found that microglia depletion reduces insoluble but not soluble amyloid-β, challenging the view that microglia clear amyloid-β, and it is animal work rather than a treatment.
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Clinical data alone poorly predicted phenoconversion in RBD due to synucleinopathy patients.
Why it matters
This multicenter study found that presynaptic dopaminergic imaging, especially combined with clinical data, improved prediction of which patients with REM sleep behavior disorder would develop Parkinson disease or dementia with Lewy bodies. Clinical data alone poorly predicted this conversion.
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Microglia activation is observed in various neurodegenerative diseases.
Why it matters
This review describes how microglia can both clear pathological protein aggregates and, when impaired, contribute to neuroinflammation and neurodegeneration, and suggests strategies such as enhancing microglial phagocytosis or reducing microglial-mediated neuroinflammation. These are proposed approaches, not proven treatments, cures or prevention for Alzheimer's disease.
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Once-weekly 5-mg/d donepezil TDS demonstrated minimal skin irritation under conditions of use of 3 consecutive weekly patch applications to the same skin site and minimal sensitization potential.
Why it matters
A once-weekly donepezil skin patch caused little skin irritation and low sensitization in healthy volunteers. This only addresses how well the patch is tolerated, not whether it improves Alzheimer's symptoms.
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Medical imaging provides numerous insights into the subclinical changes that precede serious diseases such as heart disease and dementia.
Why it matters
This study used multi-organ imaging to find cross-sectional relationships across the heart, brain, and liver in UK Biobank participants. It does not show that treating heart or liver conditions prevents dementia, and the findings are cross-sectional associations.
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Data-driven WMH spatial patterns reflect discrete underlying etiologies including arteriolosclerosis, CAA, AD, and normal aging.
Why it matters
This cross-sectional study found that white matter hyperintensities in different brain locations were linked to different causes of small vessel disease, such as probable cerebral amyloid angiopathy for juxtacortical patterns and arteriolosclerosis risk factors for deep frontal patterns. It does not test any treatment, cure or prevention, so it offers no direct guidance for managing Alzheimer's disease.
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Heterozygosity of the KL-VS haplotype has been associated with reduced amyloid and tau burden.
Why it matters
This case-control study measured Klotho concentrations in cerebrospinal fluid and plasma and related them to KL-VS heterozygosity and amyloid and tau burden in cognitively healthy controls and patients with Alzheimer disease. It investigates a possible protective factor but does not show that Klotho itself can treat or prevent the disease.
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Genetic studies have highlighted microglia as pivotal in orchestrating Alzheimer's disease (AD).
Why it matters
In mice, microglia lacking the SYK protein could not encase amyloid plaques, which worsened brain pathology and behavioral deficits. This identifies a signaling pathway involved in microglial response to amyloid, but it is animal work and not a treatment.
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Brain macrophage populations include parenchymal microglia, border-associated macrophages, and recruited monocyte-derived cells; together, they control brain development and homeostasis but are also implicated in aging pathogenesis and neurodegeneration.
Why it matters
In mice, the disease-associated microglia population seen in Alzheimer's models was found to consist of two distinct cell lineages, one of them TREM2-dependent. This refines understanding of brain immune cells in aging and neurodegeneration but is animal work with no treatment tested.
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In DIAD, clinical disease stage and BDNF Met66 were associated with cognitive impairment and levels of site-specific tau phosphorylation.
Why it matters
In dominantly inherited Alzheimer's disease, carriers of the BDNF Met66 variant showed poorer memory and cognition and higher levels of phosphorylated tau than Val66 homozygotes, both before and after symptoms appeared. The authors suggest that boosting neurotrophic support in presymptomatic stages might help, but this is a suggestion from an observational cohort study, not evidence that any treatment works.
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Our findings elucidate the predictive values of environmental factors and comorbid conditions in identifying RBD patients at higher risk of phenoconversion.
Why it matters
This study followed people with a sleep disorder to see who developed neurodegenerative disease, including dementia. It found that older age and use of nitrate derivatives were linked to higher risk, while some other factors were linked to lower risk, but it does not test any treatment or cure for Alzheimer's disease.
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Tau (MAPT) drives neuronal dysfunction in Alzheimer disease (AD) and other tauopathies.
Why it matters
This study mapped how tau interacts with synaptic and mitochondrial proteins in human stem-cell-derived neurons, and found that FTD mutations impaired bioenergetics and reduced tau's interaction with mitochondrial proteins. It is a laboratory study and does not test any treatment or prevention for Alzheimer's disease, so it has no direct implications for treating, curing, or preventing the disease.
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Total tau protein (T-Tau) and neurofilament light chain (NfL) have emerged as candidate plasma biomarkers of neurodegeneration, but studies have not compared how these biomarkers cross-sectionally or longitudinally associate with cognitive and neuroimaging measures.
Why it matters
This study compared two plasma biomarkers, neurofilament light and total tau, for their links to cognitive and brain imaging measures in people without dementia. It is about biomarkers and does not report any treatment, cure, or prevention for Alzheimer's disease.
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The abnormal aggregation of TAR DNA-binding protein 43 kDa (TDP-43) in neurons and glia is the defining pathological hallmark of the neurodegenerative disease amyotrophic lateral sclerosis (ALS) and multiple forms of frontotemporal lobar degeneration (FTLD) 1,2 .
Why it matters
Using cryo-electron microscopy on brain tissue from two people who had ALS with FTLD, this study described the shared filament structure of aggregated TDP-43. It is a structural study of tissue from a small number of individuals and does not test any treatment or prevention for Alzheimer's disease.
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The reference standard for amyloid-PET quantification requires structural MRI (sMRI) for preprocessing in both multi-site research studies and clinical trials.
Why it matters
This paper describes rPOP, a MATLAB-based pipeline that processes amyloid-PET scans without needing structural MRI, using non-linear warping and differential smoothing for any FDA-approved radiotracer. This tool allows users to perform their own quantification of amyloid-PET data in community-acquired settings.
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We analyzed data from 462 ADNI participants without dementia who underwent Aβ ([ 18 F]florbetapir or [ 18 F]florbetaben) and tau ([ 18 F]flortaucipir) PET, structural MRI, and cognitive testing.
Why it matters
This study examined how two versions of the APOE gene, ε2 and ε4, relate to amyloid-beta and tau buildup in the brains of older people without dementia, as measured by PET scans. Understanding these genetic links may help clarify why some people are more vulnerable to Alzheimer's-related brain changes.
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In mild cognitive impairment (MCI) due to Alzheimer disease (AD), also known as prodromal AD, there is evidence for a pathologic shortage of uridine, choline, and docosahexaenoic acid [DHA]), which are key nutrients needed by the brain.
Why it matters
This narrative review argues that people with mild cognitive impairment due to Alzheimer's disease may lack uridine, choline, and DHA, and that combining these nutrients is worth studying. It cites one randomized trial in prodromal Alzheimer's disease in which a multinutrient intervention slowed brain atrophy and improved some cognition measures, but this is a review, not proof of a cure or prevention.
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APOE4 is the strongest genetic risk factor associated with late-onset Alzheimer's disease (AD).
Why it matters
In lab-grown human brain organoids, the APOE4 gene variant worsened synapse loss, tau pathology and cell death compared with APOE3. Converting APOE4 to APOE3 reduced these effects, suggesting APOE4-related pathways as possible targets, but this is early laboratory work, not a treatment.
From across this topic
10 of the 4,748 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.
- Detection of Brain Tau Pathology in Down Syndrome Using Plasma Biomarkers
- Tau deposition is associated with functional isolation of the hippocampus in aging
- Sequence of Deposition of Heterogeneous Amyloid β-Peptides and APO E in Down Syndrome: Implications for Initial Events in Amyloid Plaque Formation
- Presenilin-1 Familial Alzheimer Mutations Impair γ-Secretase Cleavage of APP Through Stabilized Enzyme–Substrate Complex Formation
- Molecular mechanisms underlying nucleotide repeat expansion disorders
- Cerebral small vessel disease: The impact of glymphopathy and sleep disorders
- Alpha-synuclein inclusions in amygdala in the brains of patients with the parkinsonism-dementia complex of Guam
- Transgenic mice carrying a human mutant superoxide dismutase transgene develop neuronal cytoskeletal pathology resembling human amyotrophic lateral sclerosis lesions
- The blood-brain barrier: an overview: structure, regulation, and clinical implications
- A comprehensive analysis of deletions, multiplications, and copy number variations in PARK2