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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The molecules released into CSF, namely APOE2 for any dementia, APOE2 and Siglec-3 for AD, APOE2 for vascular dementia, and APOE2 for DLB, might be potential biomarkers.
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Amyloid plaques are a neuropathologic hallmark of Alzheimer's disease (AD), which can be imaged through positron emission tomography (PET) technology using radiopharmaceuticals that selectively bind to the fibrillar aggregates of amyloid-β plaques (Amy-PET).
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The retinal reflectance spectra in the 450-585 nm wavelengths exhibited a significant difference in individuals with increasing brain amyloid.
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With the aging of the global population, the health care burden of Alzheimer's disease (AD) and dementia is considered to increase dramatically in the coming decades.
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Anti-amyloid therapies (AATs), such as anti-amyloid monoclonal antibodies, are emerging treatments for people with early Alzheimer's disease (AD).
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Plasma biomarkers could revolutionize many areas of the AD diagnostic pathway and care continuum, but further research is needed.
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Alzheimer's disease (AD) is a progressive neurodegenerative disorder that primarily affects the elderly population.
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Early detection and timely intervention play a vital role in the effective management of Alzheimer's disease.
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Our data suggest that AD-related biomarkers are altered by food intake.
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Recently, low-sensitive plasma assays have been replaced by new ultra-sensitive assays such as single molecule enzyme-linked immunosorbent assay (Simoa), the Mesoscale Discovery (MSD) platform, and immunoprecipitation-mass spectrometry (IP-MS) with higher accuracy in the determination of plasma biomarkers of Alzheimer's disease (AD).
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The blood-brain barrier (BBB) protects the brain but is also an important obstacle for the effective delivery of therapeutics in Alzheimer's disease and other neurodegenerative disorders.
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These findings show that sleep loss alters some plasma AD biomarkers by lowering brain clearance mechanisms and needs to be taken into account when interpreting individual plasma AD biomarkers but not ratios.
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Antibody-mediated removal of aggregated β-amyloid (Aβ) is the current, most clinically advanced potential disease-modifying treatment approach for Alzheimer's disease.
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Our findings support a role for plasma GFAP as a clinical biomarker of Aβ-related astrocyte reactivity that is associated with cognitive decline and neurodegeneration.
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Measurement of Aβ in plasma contributes to addressing the amyloid component of the ATN (amyloid/tau/neurodegeneration) framework and could be a first step before or in place of a PET or cerebrospinal fluid screening study.
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Alzheimer's Disease (AD) is a progressive neurodegenerative disease characterized by amyloid-β (Aβ) plaque deposition and neurofibrillary tangle accumulation in the brain.
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In the 115 years since the discovery of Alzheimer's disease (AD), our knowledge, diagnosis, and therapeutics have significantly improved.
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The past few years have seen an explosion in sensitive and specific assays for cerebrospinal fluid (CSF) and blood biomarkers for Alzheimer's disease (AD) and related disorders, as well as some novel assays based on pathological seed-induced protein misfolding in patient samples.
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Our results suggest that pericyte injury contributes to AD progression in the early stage in an Aβ-independent pathway.
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Recent studies highlight phosphorylated tau (p-tau) at threonine tau 217 (p-tau217) as a new promising plasma biomarker for pathological changes implicated in Alzheimer's disease (AD), but the specific brain pathological events related to the alteration in p-tau217 plasma levels are still largely unknown.
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Perivascular spaces (PVS) are compartments surrounding cerebral blood vessels that become visible on MRI when enlarged.
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Abnormally phosphorylated tau, an indicator of Alzheimer's disease, accumulates in the first decades of life in the locus coeruleus (LC), the brain's main noradrenaline supply.
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Neurodegenerative disorders such as Alzheimer's disease (AD) represent a mounting public health challenge.
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For many years, blood-based biomarkers for Alzheimer's disease seemed unattainable, but recent results have shown that they could become a reality.
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43/100
Biomarkers of neurodegeneration and neuronal injury have the potential to improve diagnostic accuracy, disease monitoring, prognosis, and measure treatment efficacy.
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.
- Plasma biomarker profiles in autosomal dominant Alzheimer's disease
- LATE-NC Stage 3: a diagnostic rubric to differentiate severe LATE-NC from FTLD-TDP
- Brain metabolic correlates of cerebrospinal fluid beta-amyloid 42 and tau in Alzheimer's disease
- Cerebrospinal Fluid Aβ40 Improves the Interpretation of Aβ42 Concentration for Diagnosing Alzheimer's Disease
- Combining plasma p-tau231 and glial fibrillary acidic protein produces higher discriminative accuracy for amyloid positivity than other blood-based biomarker combinations
- Cerebral Small Vessel Disease: A Review Focusing on Pathophysiology, Biomarkers, and Machine Learning Strategies
- Tau Positron-Emission Tomography in Former National Football League Players
- Scalable plasma and digital cognitive markers for diagnosis and prognosis of Alzheimer's disease and related dementias
- Plasma p-tau212: antemortem diagnostic performance and prediction of autopsy verification of Alzheimer's disease neuropathology
- Drusen in the Peripheral Retina of the Alzheimer's Eye