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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Frontotemporal lobar degeneration (FTLD) is a common cause of early-onset dementias marked by progressive declines in behavior, cognition, and/or movement.
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Complement-mediated neuroinflammation has been implicated in Alzheimer’s disease (AD), but its role during the pre-symptomatic phase of the disease remains unclear.
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Electrochemical biosensors offer a promising route for the rapid, non-invasive detection of disease biomarkers by converting biochemical interactions into measurable electrical signals.
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Biological definitions of neuronal α-synuclein disease are advancing diagnosis beyond traditional clinical syndromes, but the trajectories preceding dementia and the influence of concomitant Alzheimer pathology remain uncertain.
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PTGDS followed a biphasic astrocytic trajectory with a statistically resolved donor-level inflection (quadratic term −2.27, p = 0.006; vertex at pseudo-progression score 0.47, bootstrap 95% confidence interval 0.32 to 0.53).
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CSF Aβ42 rose from 526.0 to 1053.0 pg/mL (+ 100.2%), total tau (t-tau) fell from 578.2 to 278.0 pg/mL(-51.9%), and phosphorylated tau181 (p-tau181) fell from 90.8 to 23.1 pg/mL(-74.6%).
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The medial temporal lobe (MTL) is crucial for episodic memory.
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Brain perfusion SPECT revealed AD-typical hypoperfusion patterns and demonstrated modest potential to estimate the presence or absence of Aβ deposition with left parietal rCBF.
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Alzheimer’s disease (AD) pathology develops years in advance prior to its clinical presentation.
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Structured Abstract INTRODUCTION Tau pathology typically occurs in Alzheimeŕs disease (AD), however is also frequently present in Parkinsońs disease dementia (PDD) and Dementia with Lewy Bodies (DLB), yet its disease-specific signature is unclear.
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Chimpanzees share a number of age-related brain changes with humans, such as reductions in neurons and increases in neuropathology.
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Ninety-six non-artifactual Amyloid-Tau components were identified, of which 73 showed appreciable spatial correspondence between their paired Amyloid and Tau maps, while 17 were Tau-localized and 6 Amyloid-localized.
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Alzheimer’s disease (AD) pathology is increasingly recognized to manifest in the retina, offering a non-invasive window for early biomarker discovery.
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Concordance between p-tau217 and Aβ was high in the AD and MCI groups (observed agreement 90.0% in each), but overall agreement across Cohort II was modest (166/351, 47.3%; Cohen's κ = 0.117, 95% CI 0.029–0.204).
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Social isolation was associated with elevated blood-based biomarkers of neuronal injury, with variation by patterns of exposure over time.
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STRUCTURED ABSTRACT BACKGROUND Chronological age and plasma p⍰tau217 each predicts cognitive decline, but whether their prognostic associations interact is unclear.
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This study investigated whether WM measures derived from amyloid-PET are associated with AD biomarkers and to determine whether they offer added diagnostic and prognostic value beyond established biomarkers.
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Alzheimer’s disease and cerebral amyloid angiopathy are characterized by the accumulation of amyloid-β (Aβ) species, yet the human fluid-physiological mechanisms that regulate soluble Aβ transport and clearance remain poorly understood.
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All three frameworks recognized biologically coherent AD-related signal despite differences in training cohort and assay methodology.
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Bidirectional stepwise linear regression analysis was performed to identify plasma biomarkers associated with brain Aβ deposition.
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As the world's population ages, Alzheimer's disease (AD), a progressive neurodegenerative disorder, is becoming more common.
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Amyloid regional extent and tau PET were associated with different features of dyadic CFI data: reporter balance and CFI burden across reporters, respectively.
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Residualized WMH T1w/T2w-FLAIR ratio captures lesion-specific microstructural variation missed by volumetric measures, consistent with vascular-gliotic injury in VD and coexisting amyloid-linked demyelination in AD.
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Our findings suggest that serum brain-derived p-tau 217 and SV2A are more specific diagnostic biomarkers for reflecting brain damage and may not be disturbed by peripheral damage for AD patients.
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Test-retest reliability measures are essential for interpretation of meaningful effects over time for plasma and digital outcomes.