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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Despite reductions in plasma p-tau217 with donanemab treatment, this biomarker cannot currently be used to accurately detect TRAC by PET (< 24.1 CL) in individuals with early symptomatic AD.
Why it matters
This analysis of the TRAILBLAZER-ALZ 2 trial found that plasma p-tau217 performed suboptimally in detecting amyloid clearance by PET after donanemab treatment, with an area under the ROC curve of 0.61 at 52 weeks. The authors conclude that this biomarker cannot currently be used to accurately detect treatment-related amyloid clearance in people with early symptomatic Alzheimer's disease.
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The long-term efficacy of amyloid-targeting therapies hinges on their ability to slow downstream neuropathologic change, but little is known about the influence of amyloid clearance on tau pathology and neurodegeneration.
Why it matters
This single-patient clinicopathologic case report examined the postmortem and in vivo association between amyloid levels and downstream neuropathology after aducanumab treatment in a man in his 50s with mild cognitive impairment who carries the p.R47H TREM2 variant. Because it describes only one patient, it cannot establish how amyloid clearance affects tau pathology and neurodegeneration more broadly.
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This study aimed to identify lipid species associated with MPH response and explore lipid pathway disruptions in responders versus non-responders.
Why it matters
Using data from the ADMET 2 trial of methylphenidate for apathy in Alzheimer's, researchers looked for lipid (fat) molecules linked to treatment response. Of 43 treated participants, 28 were responders on an apathy scale and 10 on a clinician's overall rating, and responders showed disruptions in ceramide and glycosphingolipid metabolism. The aim was to find lipid markers that could flag who is likely to respond, but the record does not report how well they predict this.
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A total of 322 participants with p-tau217, GFAP, and NfL analyses were stratified into the EOAD or FTD group based on their diagnosis.
Why it matters
In 245 people with early-onset Alzheimer's disease, higher baseline p-tau217, GFAP and neurofilament light were each linked to faster decline in cognitive scores, and all three markers rose over time. In the 77 people with frontotemporal dementia, GFAP and neurofilament light were linked to decline but p-tau217 was not.
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Baseline 18F-MK-6240 PET showed a minimal signal in CU participants, localized signal to the medial temporal lobe in participants with MCI, and a signal spanning the inferolateral temporal lobe and extending posteriorly along the ventral cortex in participants with AD.
Why it matters
This study used a tau PET tracer to track tau buildup over time in people at different stages of Alzheimer's disease, and found that tau accumulation correlated with cognitive decline. It is a brain imaging study for monitoring disease progression and does not test any treatment, cure, or prevention.
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54/100
For detecting AD-dementia, the ensemble model achieved the area under the receiver operating characteristic curve (AUROC) of 0.943 (95% confidence interval, 0.906-0.980), 0.786 (95% confidence interval, 0.673-0.899), and 0.795 (95% confidence interval, 0.716-0.874) in the internal validation, External-1, and External-2, respectively.
Why it matters
This study reports that an artificial intelligence model using eye scans could help detect Alzheimer's dementia and early-stage Alzheimer's, potentially during eye appointments. It is a diagnostic approach only and does not test any treatment, cure or prevention.
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Anosognosia, the lack of awareness of memory decline, and Neuropsychiatric Symptoms (NPS) are prevalent and debilitating symptoms in Alzheimer's disease (AD) dementia.
Why it matters
In this exploratory study, patients with Alzheimer's dementia who lacked awareness of their memory decline had a faster onset of apathy than those who were aware. There were no significant differences in the frequency of neuropsychiatric symptoms at the start, so these findings are preliminary.
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In the whole cohort, p ‐tau217, NfL, GFAP and p ‐tau181 were significantly increased over time showing more accelerated increase in Aβ+ than Aβ‐ participants.
Why it matters
In this longitudinal study, several plasma biomarkers rose over time and their rates of change tracked cognitive decline, especially in amyloid-positive participants. This supports using these markers to monitor disease progression in trials, but it does not show that any treatment changes these markers or outcomes.
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) within the first intron of SCN8A on chromosome 12 (Figure 1), overlapping a significant region in the previous admixture mapping analysis. eHiCA revealed more and stronger interactions between rs4761988 and SLC4A8, SCN8A and FIGNL2 in EU compared to AF genome (Figure 2), consistent with the admixture mapping result.
Why it matters
This genetic study in Puerto Ricans found a significant association between SCN8A and Alzheimer disease and replicated eight known Alzheimer loci. It identifies a possible new genetic factor but does not provide a treatment or cure.
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Controversies over anti-amyloid immunotherapies underscore the need to elucidate their mechanisms of action.
Why it matters
In a human microglia xenograft mouse model, lecanemab reduced amyloid-beta pathology and associated neuritic damage, and this effect did not occur when the Fc fragment was silenced or microglia were deficient. Because this is animal and cell-based work, it explains how lecanemab may clear amyloid through microglia rather than demonstrating a clinical benefit in people.
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Novel plasma assays enabled accurate blood-based biomarkers for neurodegenerative diseases with minimally invasive options for clinical use.
Why it matters
Using a large mixed-dementia cohort, this study identified many plasma proteins associated with Alzheimer's and other neurodegenerative diseases and with Alzheimer-related brain measures. These findings are about developing blood-based biomarkers for diagnosis, not about treating, curing, or preventing the disease.
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The findings suggest that permeability of the blood-brain barrier is linked to AD pathophysiology, contributes to cerebrovascular lesions observed on MRI, and is associated with neuroinflammation in middle age.
Why it matters
In 488 middle-aged adults, blood markers of blood-brain barrier permeability were linked to markers of Alzheimer pathology, cerebrovascular lesions, and neuroinflammation. This is an observational study and does not show that any treatment, cure, or prevention follows from these links.
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Plasma p‐tau 217 offers a cost‐effective AD‐specific alternative to tau‐PET and could potentially be implemented for monitoring cognitive changes in AD trials, while amyloid‐PET lacks utility.
Why it matters
Comparing different Alzheimer's biomarkers over time, this study found that tau-PET, plasma p-tau217 and cortical thickness changes tracked cognitive decline accurately, while amyloid-PET changes did not. The authors conclude that plasma p-tau217 offers a cost-effective, Alzheimer's-specific alternative to tau-PET that could potentially be used for monitoring.
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54/100
Of 31 028 older adults in MEPS, 5184 (10%) were African American; 146 (<1%) American Indian or Alaska Native; 1043 (3%) Asian (Indian, Chinese, or Filipino); 5346 (10%) Latino; 690 (2%) Other Asian, Native Hawaiian, and Pacific Islander; and 18 617 (75%) were White.
Why it matters
This study projected that the economic burden of Alzheimer disease and related dementias will rise from close to $344 billion in 2020 to over $3 trillion in 2060, with African American and Latino adults bearing a disproportionate share. The authors suggest understanding prevalence, comorbidity, inadequate care, and support policies may reduce these burdens.
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Amyloid burden impacts cognitive decline in the pre-dementia stages of Alzheimer's disease (AD), but there remains significant variability in cognitive trajectories that may be explainable by markers of synaptic function and neurodegeneration.
Why it matters
In a longitudinal study of 434 at-risk but mostly unimpaired people, higher levels of the synaptic protein NPTX2 were linked to slower cognitive decline even in those with amyloid buildup. This identifies NPTX2 and a SNAP-25/NPTX2 ratio as possible markers of synaptic function, not as a treatment or cure.
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These findings highlight LBP prevalence in DSAD but suggest current SAA may fail to detect limited αSyn deposition.
Why it matters
In cerebrospinal fluid from 270 adults with Down syndrome, an alpha-synuclein seed amplification assay was positive in 9.2% of cases, and Lewy body pathology was found in 47% of necropsies. The authors suggest the current assay may fail to detect limited alpha-synuclein deposition, so this is about measuring co-pathology, not treating or preventing Alzheimer's disease.
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Observational studies and pilot trials suggest that metformin may help prevent cognitive decline in neurodegenerative disorders.
Why it matters
This is a protocol for a phase II/III trial testing extended-release metformin against placebo in 326 people with amnestic mild cognitive impairment without diabetes. It notes that an earlier small trial of short-acting metformin showed preliminary evidence of safety and efficacy, but the current trial's results are not yet available.
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The study cohort comprised a total of 6108 individuals diagnosed with AD dementia during the study period (28.4% males and 71.6% females).
Why it matters
In a large memory unit cohort, cognitive decline was largely similar between men and women with Alzheimer's dementia, though women with mild dementia progressed faster on one measure. The authors say their findings do not strongly support sex significantly modifying clinical progression and call for further research.
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Our study provides evidence that plasma p-tau217 has strong discriminative accuracy for AD among patients with early-onset and/or atypical dementia assessed in specialized settings.
Why it matters
In 81 people with early-onset or atypical dementia, a blood test for p-tau217 identified Alzheimer's disease biomarker profiles more accurately than visual reading of FDG-PET scans. The authors call for these findings to be replicated in other care settings before use in practice.
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Our results demonstrate that unsupervised digital memory assessments might be used for diagnosis and prognosis in Alzheimer's disease, potentially in combination with plasma biomarkers.
Why it matters
Remote memory tests done by people at home on mobile devices were usable, valid, and reliable, and were linked to tau PET scans and brain MRI measures, and memory performance predicted future cognitive decline, especially when combined with a blood marker called plasma p-tau217. This study is about improving diagnosis and prognosis, not about treating, curing or preventing Alzheimer's disease.
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Ten papers were identified from 7 studies.
Why it matters
This review of 10 papers found little evidence linking amyloid PET disclosure to depression, but people with mild cognitive impairment and their caregivers who had elevated amyloid had increased risk of distress or anxiety. It found mixed evidence on psychosocial and behavioral outcomes and no studies measuring behavioral outcomes.
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54/100
Alzheimer's Disease (AD) contributes to most cases of dementia.
Why it matters
This review notes that amyloid-targeting therapies have been the focus of drug development and that two such drugs received accelerated FDA approval, but their efficacy or long-term safety remains uncertain. It reports no established cure or prevention.
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Alzheimer's disease (AD), the most common cause of dementia, results in a sustained decline in cognition.
Why it matters
This review discusses the gut microbiome as a possible upstream modulator of amyloid, tau and neuroinflammation in Alzheimer's disease, while noting there are currently few effective disease-modifying therapies. It offers no confirmed treatment, cure or prevention.
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CSF biomarkers β-amyloid 1-42 (Aβ 42 ), phosphorylated tau 181 (p-tau 181 ), total tau (t-tau), and neurogranin (Ng) can diagnose Alzheimer disease (AD) in life.
Why it matters
This study checked whether having both Alzheimer's and alpha-synuclein pathology at autopsy changes CSF levels of amyloid, tau and neurogranin. It is about whether these biomarkers remain accurate when another brain disease is also present, not about treatment.
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Alzheimer's disease (AD) is the most common cause of dementia worldwide, and its prevalence is rapidly increasing due to extended lifespans.
Why it matters
This review describes how the APOE gene, especially the ε4 allele, increases Alzheimer's disease risk while the ε2 allele is protective, and how apoE relates to amyloid-beta. It discusses challenges in designing apoE-targeted therapeutic strategies but reports no proven treatment or cure.
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.
- White matter hyperintensities and cerebral amyloidosis: necessary and sufficient for clinical expression of Alzheimer disease?
- Amyloid deposition and influx transporter expression at the blood-brain barrier increase in normal aging
- Is cognitive training an effective treatment for preclinical and early Alzheimer's disease?
- Large Soluble Oligomers of Amyloid β-Protein from Alzheimer Brain Are Far Less Neuroactive Than the Smaller Oligomers to Which They Dissociate
- Evaluation of CSF-tau and CSF-Abeta42 as diagnostic markers for Alzheimer disease in clinical practice
- Is Alzheimer's Disease Risk Modifiable?
- Amyloid precursor protein in platelets of patients with Alzheimer disease: effect of acetylcholinesterase inhibitor treatment
- Participation in cognitively stimulating activities and risk of incident Alzheimer disease
- Olfaction and Plasma Biomarkers of Alzheimer Disease and Neurodegeneration in the Atherosclerosis Risk in Communities Study
- Reliable New Biomarkers of Mitochondrial Oxidative Stress and Neuroinflammation in Cerebrospinal Fluid and Plasma from Alzheimer’s Disease Patients: A Pilot Study