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biomarkers
854 studies tagged biomarkers, dated 1980-07-01 to 2026-10-16. Bibliography: BibTeX (.bib) · RIS (.ris)
Newest in this topic
Studies
854 studies carry this tag.
Date range
1980 to 2026
Top journals
- Neurology 131
- Alzheimer s & Dementia 37
- JAMA neurology 35
- Alzheimer's research & therapy 28
- Archives of neurology 25
251 journals in all.
Newest first, then by address. Each study has a usefulness score out of 100 (rubric version 4.0); tap a score to see what makes it up. Tags were assigned automatically from each study's title and summary. The same studies as a filter in the library.
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These findings suggest that although WMH are primarily related to systemic vascular risk and neurodegeneration (i.e., t-tau), AD-specific pathways may contribute to the formation of WMH in a regionally-specific manner, with neurofibrillary tangles (i.e., p-tau) playing a role in temporal WMHs and amyloid (i.e., Aβ 42/Aβ 40) in parietal WMHs.
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The temporal evolutions and relative orderings of Alzheimer disease biomarkers, including CSF amyloid-β42 (Aβ42), Aβ40, total tau (Tau) and phosphorylated tau181 (pTau181), standardized uptake value ratio (SUVR) from the molecular imaging of cerebral fibrillar amyloid-β with PET using the 11C-Pittsburgh Compound-B (PiB), MRI-based hippocampal volume and cortical thickness and cognition have been hypothesized but not yet fully tested with longitudinal data for all major biomarker modalities among cognitively normal individuals across the adult lifespan starting from 18 years.
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Among cognitively normal participants with positive biomarkers, 34.4% developed cognitive impairment (Clinical Dementia Rating > 0) as compared to 8.4% of those with negative biomarkers.
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Performance was assessed in comparison to clinical diagnosis (blinded to plasma results) and amyloid status (CSF/PET).
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48/100
Our study revealed the possibility of urinary formic acid as a potential novel biomarker for the early diagnosis of AD.
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Blood biomarkers showed significant longitudinal changes corresponding to cognitive decline, clinical AD, and structural MRI characteristics.
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50/100
Brain Aβ deposition is a key early event in the pathogenesis of Alzheimer´s disease (AD), but the long presymptomatic phase and poor correlation between Aβ deposition and clinical symptoms remain puzzling.
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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.
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CSF markers of iron and neuroinflammation have distinct associations with disease stages, while iron may be more intimately associated with apolipoprotein E and tau pathology.
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51/100
Our results support the utility of CSF VEC as a marker of endothelial injury in AD and highlight the importance of endothelial injury as an early pathology that contributes to cognitive impairment in even the earliest preclinical stages.
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Sleep abnormalities are prevalent in Alzheimer's disease, with sleep quality already impaired at its preclinical stage.
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Alzheimer's disease CSF biomarkers 42 amino acid long amyloid-β peptide (Aβ1-42), total tau protein (T-tau), and tau protein phosphorylated at threonine 181 (P-tau181) are considered surrogate biomarkers of Alzheimer's disease pathology, and significantly improve diagnostic accuracy.
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These findings suggest an association of sHHV infection with white matter volume loss, attentional decline, and astrogliosis.
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We retrospectively assessed participants with atypical and/or early-onset dementia evaluated at a tertiary care memory clinic.
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Overall, 2,277 individuals had at least 1 baseline blood biomarker available (n = 357 for CSF subsample, n = 649 for PET subsample), among whom 257 were diagnosed with clinical AD/mixed dementia during follow-up.
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To test whether cerebrospinal fluid (CSF) growth-associated protein 43 (GAP-43) concentration is elevated in Alzheimer's disease (AD) dementia and its associations with other hallmarks of AD, we examined the CSF GAP-43 measurements of 787 participants (245 cognitively normal (CN), 415 individuals with mild cognitive impairment (MCI) and 127 individuals with AD dementia) from the Alzheimer's Disease Neuroimaging Initiative (ADNI) study.
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Autoantibody-associated psychiatric syndromes are a novel disease entity that is not fully understood.
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In this retrospective study, GAP-43 was measured in participants from the AD Neuroimaging Initiative (ADNI) cohort using an in-house ELISA method, and levels were compared between groups, both cross-sectionally and longitudinally.
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In this cross-sectional study of plasma biomarkers by race and genetic ancestry, the results indicated that plasma p-tau181, Aβ40, and NFL were lower in African American individuals based on self-reported race but not genetic ancestry.
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This study aimed to examine whether baseline CSF measures of Alzheimer disease (AD)-related pathology are associated with the time to onset of mild cognitive impairment (MCI) and whether these associations differ by age, sex, Apolipoprotein E ( ApoE4 ) status, and proximal (≤7 years) vs distal (>7 years) time to symptom onset.
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The microRNAs (miRNAs) are potential biomarkers for complex pathologies due to their involvement in the regulation of several pathways.
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Amyloid-beta 42 (Aβ42) and phosphorylated tau (pTau) levels in cerebrospinal fluid (CSF) reflect core features of the pathogenesis of Alzheimer's disease (AD) more directly than clinical diagnosis.
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We investigated whether β-amyloid, cortical thickness in medial temporal lobe structures, neuroinflammation, and sociodemographic factors were associated with greater anxious-depressive symptoms during the COVID-19 confinement.
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Genetic pathways implicated in causing AD are related to altered levels of soluble tau through both Aβ-dependent and Aβ-independent mechanisms, which may have relevance for anti-tau drug development.
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51/100
Determining blood biomarkers represents less invasive and less costly diagnostics for Alzheimer´s disease.
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Extracellular plaques composed of the hydrophobic peptide amyloid-β and intraneuronal accumulation of the hyperphosphorylated protein tau (p-tau) are pathological hallmarks found in the brains of most people affected by Alzheimer's disease (AD).
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Autoimmune encephalitis (AE) is a potentially treatable cause of rapidly progressive dementia that may mimic Creutzfeldt-Jakob disease (CJD).
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62/100
Although recent studies have demonstrated the prognostic utility of plasma biomarkers of Alzheimer pathology or neurodegeneration, such as pTau-181 and NF-L, whether other plasma biomarkers can further improve prediction of cognitive decline is undetermined.
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This review addresses recent developments in the analyses of plasma amyloid beta (Aβ) and total tau (t-tau) protein levels as biomarkers for discriminating amnestic mild cognitive impairment (aMCI) from Alzheimer disease (AD), using immunomagnetic reduction (IMR).
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The proposed novel, pragmatic method to determine CSF biomarker cutoffs for AD does not require assessment of other biomarkers or assumptions concerning the clinical diagnosis of patients.
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Higher grey matter volumes/cortical thickness and fluorodeoxyglucose uptake have been consistently found in cognitively unimpaired individuals with abnormal Alzheimer's disease biomarkers compared with those with normal biomarkers.
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Several recent research studies show high performance of blood biomarkers to identify Alzheimer's disease also in the pre-dementia mild cognitive impairment (MCI) stage, but data from the routine clinical care memory clinic setting are needed.
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Blood pressure variability is an emerging risk factor for cognitive decline and dementia, but mechanisms remain unclear.
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Higher sNfL concentrations were associated with worse performance in cognitive tests at baseline, including CERAD (B = −10.084, SE = 2.999, p < 0.001) and MMSE (B = −3.014, SE = 1.293, p = 0.021).
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This study aims to quantify microglial activation in individuals with Alzheimer disease (AD) using the 18-kDa translocator protein (TSPO) PET imaging in the hippocampus and precuneus, the 2 AD-vulnerable regions, and to evaluate the association of baseline neuroinflammation with amyloidosis, tau, and longitudinal cognitive decline.
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Participants with higher total-tau and NfL at baseline had a higher risk of stroke and several stroke subtypes.
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58/100
Longitudinal racial differences in amyloid biomarkers are observed.
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CSF biomarkers, including P-tau, T-tau, Aβ 42 , Aβ 40 , and NFL, support in vivo identification of AD neuropathology and correlate with FTLD neuropathology.
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The analyzed parameters differentiate between controls and CAA with clinically useful accuracy (AUC > ∼0.85) but not between CAA and AD.
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CSF NfL is a non-specific marker of aging and white matter integrity with limited sensitivity to specific markers of AD.
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Cerebrospinal fluid (CSF) tau and beta-amyloid levels in chronic traumatic encephalopathy (CTE), a disease which can be clinically indistinguishable from Alzheimer's disease (AD), are largely unknown.
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Alzheimer disease (AD) is a leading cause of dementia that has gained prominence in our aging society.
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Age-related frailty and disease-related frailty may represent different degrees of frailty severity on a biological level.
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Experimental studies suggest that the balance between short and long β-amyloid (Aβ) species might modulate the toxic effects of Aβ in Alzheimer disease (AD), but clinical evidence is lacking.
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48/100
This study failed to find associations of circulating NfL and PGRN levels with frailty among community-dwelling older adults in adjusted analyses.
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Plasma Aβ42/Aβ40 is a robust measure for detecting amyloid plaques and can be utilized to aid in the diagnosis of AD, identify those at risk for future dementia due to AD, and improve the diversity of populations enrolled in AD research and clinical trials.
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Black Americans are disproportionately affected by dementia.
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This study suggests that plasma GFAP is a sensitive biomarker for detecting and tracking reactive astrogliosis and Aβ pathology even among individuals in the early stages of AD.
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We established AD diagnostic models using plasma biomarkers for Chinese participants.
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We previously demonstrated that PNA5, a novel glycosylated angiotensin 1-7 (Ang-(1-7)) Mas receptor (MasR) agonist peptide, is an effective therapy to rescue cognitive impairment in our preclinical model of VCID.
From across this tag
10 of the 849 studies in this tag, 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.
- Abnormal brain spectrin immunoreactivity in sprouting neurons in Alzheimer disease
- Alzheimer Disease Blood Biomarkers and Cognition Among Individuals With Diabetes and Overweight or Obesity
- Association of epigenetic aging with plasma biomarkers of amyloid, tau, neurodegeneration, and neuroinflammation in Hispanic/Latino adults
- Aβ‐reactive T cell polyfunctionality response as a new biomarker for mild cognitive impairment
- Fluid biomarkers in Alzheimer disease
- Supportive CSF biomarker evidence to enhance the National Institute on Aging-Alzheimer's Association criteria for diagnosis of Alzheimer's type dementia--a study from Southern India
- Interrelations of Alzheimer´s disease candidate biomarkers neurogranin, fatty acid-binding protein 3 and ferritin to neurodegeneration and neuroinflammation
- Neurofilament light chain and Alzheimer pathology biomarkers in elderly people with multiple sclerosis
- Indices of Arterial Stiffness and the Alzheimer’s Disease Biomarker, p-tau217, in Non-Demented Midlife Women
- Cerebrospinal Fluid Alzheimer Markers in Depressed Elderly Subjects with and without Alzheimer's Disease