ReviewMolecular psychiatry2024
Monitoring synaptic pathology in Alzheimer's disease through fluid and PET imaging biomarkers: a comprehensive review and future perspectives.
Review in Molecular psychiatry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The trial behind it
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Who cites it
22 citing papers in PubMed.
- ABBV-552 in patients with mild Alzheimer's disease: a randomized phase IIb trial.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Trial
- Sex-Specific Relationships Between Nociceptin/Orphanin FQ Peptide (NOP) Receptors and Alcohol Drinking: Longitudinal PET Studies in Cynomolgus Monkeys.Basic & clinical pharmacology & toxicology · 2026Article
- Dorsolateral Prefrontal Cortex Circuitry at the Intersection of Cognition and Disease.Biological psychiatry · 2026Review
- Elevated CSF GAP-43 is associated with reduced cerebral glucose metabolism and cognitive impairment in individuals with mild cognitive impairment.Brain imaging and behavior · 2026Article
- Higher physical activity levels mitigate synaptic protein loss and cognitive deterioration in aging and in Alzheimer's disease: a 10-year longitudinal study.Molecular biomedicine · 2026Article
- Microglia-mediated synaptic pruning in neural circuit remodeling: multidimensional control in homeostasis and neuropathology.BMC medicine · 2026Review
- Nanoparticles that target nonamyloid and nontau pathways in Alzheimer's disease.Discover nano · 2026Review
- The presynaptic protein bassoon is a biofluid biomarker of synaptic pathology in multiple sclerosis.EBioMedicine · 2026Article
- Axonopathy: mechanisms and potential therapeutic targets for neurodegenerative diseases.Translational neurodegeneration · 2026Review
- Early synaptic pathology is associated with small tau aggregates in Alzheimer's disease.Acta neuropathologica · 2026Article
- Alismatis Rhizoma prevents AβO-induced neuronal cell death and synaptic loss in Alzheimer's disease models.Frontiers in pharmacology · 2026Article
- From pathology to network failure: a Question-Model-Outcome framework for interpreting animal models of AD-related and dementia-relevant mechanisms.Frontiers in aging neuroscience · 2026Review
- Reduced synaptic vesicle protein 2A in extracellular vesicles and brains of Alzheimer's disease: associations with Aβ, tau, synaptic proteins and APOE ε4.Translational neurodegeneration · 2025Article
- Modernizing diagnosis of Alzheimer's disease: A review of global trends and Asia-specific perspectives.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Psychoactive substances: novel molecular insights and therapeutic potential for Alzheimer's disease.Translational neurodegeneration · 2025Review
- From Amyloid to Synaptic Dysfunction: Biomarker-Driven Insights into Alzheimer's Disease.Current issues in molecular biology · 2025Review
- Synapse vulnerability and resilience across the clinical spectrum of dementias.Nature reviews. Neurology · 2025Review
- Early increase of the synaptic blood marker β-synuclein in asymptomatic autosomal dominant Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Generating synthetic brain PET images of synaptic density based on MR T1 images using deep learning.EJNMMI physics · 2025Article
- Dual GSK3β/SIRT1 modulators for Alzheimer's: mechanisms, drug discovery and future perspectives.Frontiers in pharmacology · 2025Review
Corrections and comments
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is currently constrained by limited clinical treatment options. The initial pathophysiological event, which can be traced back to decades before the clinical symptoms become apparent, involves the excessive accumulation of amyloid-beta (Aβ), a peptide comprised of 40-42 amino acids, in extraneuronal plaques within the brain. Biochemical and histological studies have shown that overaccumulation of Aβ instigates an aberrant escalation in the phosphorylation and secretion of tau, a microtubule-binding axonal protein. The accumulation of hyperphosphorylated tau into intraneuronal neurofibrillary tangles is in turn correlated with microglial dysfunction and reactive astrocytosis, culminating in synaptic dysfunction and neurodegeneration. As neurodegeneration progresses, it gives rise to mild clinical symptoms of AD, which may eventually evolve into overt dementia. Synaptic loss in AD may develop even before tau alteration and in response to possible elevations in soluble oligomeric forms of Aβ associated with early AD. These findings largely rely on post-mortem autopsy examinations, which typically involve a limited number of patients. Over the past decade, a range of fluid biomarkers such as neurogranin, α-synuclein, visinin-like protein 1 (VILIP-1), neuronal pentraxin 2, and β-synuclein, along with positron emission tomography (PET) markers like synaptic vesicle glycoprotein 2A, have been developed. These advancements have facilitated the exploration of how synaptic markers in AD patients correlate with cognitive impairment. However, fluid biomarkers indicating synaptic loss have only been validated in cerebrospinal fluid (CSF), not in plasma, with the exception of VILIP-1. The most promising PET radiotracer, [
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