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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CL was associated with syndromic (F = 4.42, p = 0.014) and etiological diagnosis (F = -12.66, p < 0.001), with Alzheimer's disease (AD) patients showing the highest amyloid burden (62.9 ± 27.5), followed by dementia with Lewy bodies (DLB) (25.3 ± 35.5) and cardiovascular disease (CVD) (16.7 ± 24.5), and finally frontotemporal lobe degeneration (FTLD) (5.0 ± 17.22, t = -12.66, p < 0.001).
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Of 136 patients, 40 and 50 patients developed PSCI at 3 and 12 months after stroke, respectively.
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Current evidence shows that plasma p-tau217 is a sensitive maker of the clinical manifestation and progression of Alzheimer's disease and of pathological changes associated with this condition, including amyloid accumulation, tau burden, brain atrophy and physical degradation.
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Seventy-six articles met the inclusion criteria for systematic review.
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Lower CSF Aβ42, and higher t-tau/Aβ42 and p-tau/Aβ42 ratios were associated with BDI-II and BAI total scores, clinical depression (BDI-II ≥ 13), and clinical anxiety (BAI ≥ 10), as well as NPI-Q-assessed anxiety, apathy, and nighttime behavior.
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We included 401 individuals (61±9 years, 42% female, MMSE 28 ± 2, vascular comorbidities 8%-19%).
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Higher CSF NfL was associated with decreasing microstructural integrity and WMH.
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Plasma amyloid-β peptide concentration has recently been shown to have high accuracy to predict amyloid-β plaque burden in the brain.
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ROC curves of the five best two-, three-, and four-parameter combinations were analyzed for significant superiority by a bootstrapping wrapper around a support vector machine with linear kernel.
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Plasma p-tau217 showed larger fold-changes and better accuracy for detecting AD pathology in symptomatic individuals, with greater cross-platform agreement than other p-tau variants.
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Aβ-PET was abnormal in 81 participants from J-TRC and 71 participants from BioFINDER.
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Plasma p-tau217 may capture earlier Alzheimer's disease (AD)-related cognitive and brain atrophy hallmarks in females compared to males, possibly reflective of increased susceptibility to AD pathophysiology.
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69/100
Primary include several amyloid PET measurements (Centiloid, SUVr, BPND , R1 ), and secondary are their changes from baseline, relationship to other amyloid markers (cerebrospinal fluid and visual assessment), and predictive value of AD-related decline.
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Amyloid chronicity provides unique information about cognitive decline and neurofibrillary tangle development and may be useful to investigate preclinical Alzheimer's disease.
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Our results encourage an independent validation cohort study to confirm the indication that the plasma Aβ 1-40 /Aβ 1-42 ratio, assessed via Simoa, may improve future standard of care and clinical trial design.
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Subtraction MRI has potential as a visual aid increasing the sensitivity of ARIA-E assessment.
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Detection of Alzheimer's disease (AD) before the development of clinical symptoms is critical for enabling the use of new treatments.
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In participants who progressed to amyloid-positive MCI, plasma p-tau181/Aβ42 and GFAP diverged from stable controls earliest (about 13 and 12 years before symptom onset, respectively), followed by Aβ42/Aβ40, p-tau181, and NfL, all of which became abnormal before symptom onset.
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MES-defined cognitive impairment (≤-2 standard deviation [SD] deviation after adjustment for demographics) was identified in 12.4% of participants.
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We included 400 middle-aged CU participants, of whom 135 (33.8%) were CSF Aβ-positive.
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αSyn SAA positivity was more common in Aβ + vs. Aβ- subjects and increased with clinical severity (p < 0.001).
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Limbic predominant age-related TDP-43 encephalopathy neuropathologic change (LATE-NC) is highly prevalent in late life and a common co-pathology with Alzheimer's disease neuropathologic change (ADNC).
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SAA+ individuals had faster cognitive decline than SAA-, notably in mild cognitive impairment, and presented with earlier symptom onset.
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68/100
Across cohorts, the main biomarker associated with α-synuclein positivity at baseline was higher levels of Aβ pathology (all p values ≤ 0.02), but not tau.
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Brain volume analyses included 622 participants (mean age ± SD: 70.9 ± 10.2) with an average of 3.3 MRI scans over 4.7 years.
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.
- Post-mortem histopathology underlying β-amyloid PET imaging following flutemetamol F 18 injection
- Synergistic effect of β-amyloid and neurodegeneration on cognitive decline in clinically normal individuals
- Plasma p-Tau217 improves diagnostic accuracy and clinician confidence in cognitive disorder classification
- Validation of Optical Coherence Tomography Retinal Segmentation in Neurodegenerative Disease
- Portable electrochemical micro-workstation platform for simultaneous detection of multiple Alzheimer's disease biomarkers
- Tailoring thresholds for interpreting plasma p-tau217 levels
- Cortical hypometabolism reflects local atrophy and tau pathology in symptomatic Alzheimer's disease
- TDP-43 is a key player in the clinical features associated with Alzheimer's disease
- Plasma p-tau217 predicting brain-wide tau accumulation in preclinical AD
- Longitudinal stability of CSF tau levels in Alzheimer patients