ArticleMolecular psychiatry2026
Beyond amyloid and tau: synaptic and neurodegenerative biomarkers shape MCI progression.
Article in Molecular psychiatry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Menopausal insomnia as a modifiable node of dementia risk: Mechanistic insights and intervention strategies.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
Accurate prediction of which patients with mild cognitive impairment (MCI) will progress to dementia remains a major challenge. Current biomarkers detect amyloid pathology with high accuracy but offer limited prognostic value for disease progression. We conducted a prospective analysis in the multicentre BALTAZAR cohort, all diagnosed with MCI at baseline and followed for 3 years. Paired cerebrospinal fluid (CSF) and plasma samples were analysed with the NULISA ultrasensitive multiplex platform quantifying more than 120 central nervous system biomarkers. Prognostic performance was assessed using area under the curve (AUC) and hazard ratios (HRs), both for individual markers and for elastic-net-derived biomarker combinations validated by bootstrap and survival analyses. During the 3-year follow-up, 36% of participants converted to dementia. Plasma p-tau biomarkers showed strong accuracy for detecting amyloid positivity (AUC > 0.90) but limited prognostic value for conversion (AUC < 0.75). In CSF, markers of neurodegeneration (tau, NfL) and synaptic dysfunction (NPTX2 encoding the Neuronal Pentraxin 2) predicted conversion with higher accuracy, exceeding p-tau217 performance. The best-performing CSF combination (IL-16, tau, NPTX2) achieved an AUC of 0.86 (95%CI 0.80-0.91) and an HR of 39.8 (95%CI 9.6-165.2). Plasma combinations (p-tau181 or p-tau217 with YWHAG encoding for 14-3-3 protein gamma, a member of the 14-3-3 protein family) provided only modest improvement, likely reflecting the absence of robust synaptic markers in blood. Prognostic assessment of MCI progression to dementia is best achieved through CSF biomarker combinations reflecting neurodegeneration and synaptic dysfunction, complemented by inflammatory markers. These findings emphasize the clinical and pathophysiological relevance of downstream processes beyond amyloid and tau, and support the implementation of multimarker panels for prognosis and therapeutic monitoring.
Identifiers
42337011What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.