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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Neurofilaments are structural components of neurons and are particularly abundant in highly myelinated axons.
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To assess volume loss and flortaucipir uptake in patients with semantic dementia (SD) over time.
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55/100
In Alzheimer's diseases (AD), tau pathology is strongly associated with cognitive decline.
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The Lumipulse G assays show a very good analytical performance that makes them well-suited for CSF clinical routine measurements.
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These findings indicate that plasma NfL is a proxy for neurodegeneration in AD-related regions in Aβ+ subjects.
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Studies of rodent models of Alzheimer's disease (AD) and of human tissues suggest that the retinal changes that occur in AD, including the accumulation of amyloid beta (Aβ), may serve as surrogate markers of brain Aβ levels.
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Previous studies demonstrated that plasma neurofilament light chain (NFL) played important predictive roles in disease progression and neurodegeneration in the preclinical phase of familial Alzheimer's disease (AD).
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The combined model (Harrell's C = 0.82 [0.78-0.86]) was significantly superior to demographics (β = 0.100, P < .001), magnetic resonance imaging (β = 0.037, P = .011), and PET only models (β = 0.053, P = .003).The models can be used to calculate individualized risk, for example, a female MCI patient (age = 60, APOE ε4 positive, Mini-Mental State Examination = 25, hippocampal volume = 5.8 cm3, amyloid PET positive) has 35% (19-57) risk in one year and 85% (64-97) risk in three years.
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55/100
Elevated baseline plasma NfL is a prognostic marker of cognitive decline and neuroimaging measures of neurodegeneration, and has similar effect sizes to baseline CSF NfL.
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We examined the relationships between amyloid-β PET and concurrent and longitudinal cognitive performance in 107 cognitively normal individuals with subjective cognitive decline (age: 64 ± 8 years, 44% female, Mini-Mental State Examination score 29 ± 1).
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Cerebrospinal fluid (CSF) tau and phosphorylated tau (ptau) are definite biomarkers of Alzheimer's disease (AD).
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These longitudinal estimates clarify the sequence and temporal dynamics of presymptomatic pathologic changes in autosomal dominant AD, information critical to a better understanding of the disease.
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Epidemiologic and mechanistic evidence is increasingly supporting the notion that obstructive sleep apnea is a risk factor for dementia.
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Plasma a-synuclein level was significantly increased in patients with PD and APS when compared with controls and FTD without parkinsonism (p<0.01).
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These findings support the use of plasma Aβ42/40 ratios as surrogate biomarkers of cortical Aβ deposition and enrichment tools, reducing the number of subjects submitted to invasive tests and, consequently, recruitment costs in clinical trials targeting cognitively normal individuals.
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The best discriminators between probable/definite bvFTD and PSY were the levels of CSF NfL (area under the curve [AUC] 0.93, P < .001, 95% confidence interval [CI] 0.85-1.00), p-tau/tau ratio (AUC 0.87, P < .001, 95% CI 0.77-0.97), and YKL40 (AUC 0.82, P = .001, 95% CI 0.68-0.97).
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Among the nonmotor symptoms in Parkinson's disease (PD), cognitive impairment is one of the most common and devastating.
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Medial temporal lobe AV-1451 uptake distinguishes AD dementia from probable DLB, which may be useful for differential diagnosis.
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We aimed to compare [18F]-florbetaben PET imaging in four transgenic mouse strains modelling Alzheimer's disease (AD), with the main focus on APPswe/PS2 mice and C57Bl/6 mice serving as controls (WT).
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The lack of readily available biomarkers is a significant hindrance toward progressing to effective therapeutic and preventative strategies for Alzheimer's disease (AD).
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This is the first human study to demonstrate that insulin resistance may contribute to amyloid deposition in brain regions affected by AD.
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Using a targeted proteomics approach, we confirmed previous findings for a subset of markers, defined longitudinal performance of our panel of markers, and established a flexible proteomics method for robust multiplexed analyses.
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Recent developments of PET amyloid ligands have made it possible to visualize the presence of Aβ deposition in the brain of living participants and to assess the consequences especially in individuals with no objective sign of cognitive deficits.
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The hypothesis that amyloid deposition is the leading cause of Alzheimer's disease (AD) is supported by findings in transgenic animal models and forms the basis of clinical trials of anti-amyloid agents.
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Using cutoffs established from a control cohort, we found that 14 (54%) patients had increased levels of PiB retention and were considered "amyloid-positive."
From across this topic
10 of the 1,573 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.
- Polygenic risk for Alzheimer's disease is associated with neuroaxonal damage before onset of clinical symptoms
- Retinal amyloid pathology and proof-of-concept imaging trial in Alzheimer's disease
- Amyloid-β positive individuals with subjective cognitive decline present increased CSF neurofilament light levels that relate to lower hippocampal volume
- Limbic Predominant Age-Related TDP-43 Encephalopathy (LATE): Clinical and Neuropathological Associations
- Amyloid Metabolism and Amyloid-Targeting Blood-Based Biomarkers of Alzheimer's Disease
- Diagnosis of Alzheimer's disease: Towards accuracy and accessibility
- Five Decades of Infusion Testing in Idiopathic Normal Pressure Hydrocephalus: A Biomarker in Search of a Gold Standard
- Using Retinal Imaging to Study Dementia
- Plasma NfL, GFAP, and pTau181 in patients with isolated REM sleep behavior disorder
- Comparing positron emission tomography imaging and cerebrospinal fluid measurements of β-amyloid