ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006
Neuronal pentraxin 1 contributes to the neuronal damage evoked by amyloid-beta and is overexpressed in dystrophic neurites in Alzheimer's brain.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 105 citations in OpenAlex.
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- Cerebrospinal fluid neuronal pentraxin levels are associated with tau pathology via microglia-astrocyte signaling in alzheimer's disease.Journal of neuroinflammation · 2025Article
- Disturbed engram network caused by NPTX downregulation underlies aging-related contextual fear memory deficits.Cell research · 2025Article
- Glycogen synthase kinase 3 (GSK3) inhibition: a potential therapeutic strategy for Alzheimer's disease.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Structural and functional alterations of neurons derived from sporadic Alzheimer's disease hiPSCs are associated with downregulation of the LIMK1-cofilin axis.Alzheimer's research & therapy · 2024Article
- Pathogenic tau induces an adaptive elevation in mRNA translation rate at early stages of disease.Aging cell · 2024Article
- Plasma Biomarkers in Neurodegenerative Dementias: Unrevealing the Potential of Serum Oxytocin, BDNF, NPTX1, TREM2, TNF-alpha, IL-1 and Prolactin.Current Alzheimer research · 2024Article
- Monomeric C-reactive protein: A novel biomarker predicting neurodegenerative disease and vascular dysfunction.Brain pathology (Zurich, Switzerland) · 2023Review
- An interventional study of baicalin on neuronal pentraxin-1, neuronal pentraxin-2, and C-reactive protein in Alzheimer's disease rat model.Translational neuroscience · 2023Article
- A Review of Proteins Associated With Neuroprotection and Regeneration in Alzheimer's Disease.Cureus · 2022Review
- Global Proteome Profiling of the Temporal Cortex of Female Rats Exposed to Chronic Stress and the Western Diet.Nutrients · 2022Article
- The amyloid plaque proteome in early onset Alzheimer's disease and Down syndrome.Acta neuropathologica communications · 2022Article
- Neuronal pentraxins as biomarkers of synaptic activity: from physiological functions to pathological changes in neurodegeneration.Journal of neural transmission (Vienna, Austria : 1996) · 2022Review
- Sex-specific accelerated decay in time/activity-dependent plasticity and associative memory in an animal model of Alzheimer's disease.Aging cell · 2021Article
- Biological Significance of the Protein Changes Occurring in the Cerebrospinal Fluid of Alzheimer's Disease Patients: Getting Clues from Proteomic Studies.Diagnostics (Basel, Switzerland) · 2021Review
- Tau Protein Interaction Partners and Their Roles in Alzheimer's Disease and Other Tauopathies.International journal of molecular sciences · 2021Review
- Human brain region-specific variably methylated regions are enriched for heritability of distinct neuropsychiatric traits.Genome biology · 2021Article
- Apolipoprotein E4-driven effects on inflammatory and neurotrophic factors in peripheral extracellular vesicles from cognitively impaired, no dementia participants who converted to Alzheimer's disease.Alzheimer's & dementia (New York, N. Y.) · 2021Article
- Molecular mechanisms of aluminum neurotoxicity: Update on adverse effects and therapeutic strategies.Advances in neurotoxicology · 2021Article
- Tau Protein as a New Regulator of Cellular Prion Protein Transcription.Molecular neurobiology · 2020Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulation of amyloid-beta (Abeta) is thought to play a central role in the progressive loss of synapses, the neurite damage, and the neuronal death that are characteristic in brains affected by Alzheimer's disease. However, the mechanisms through which Abeta produces such neurotoxicity remain unclear. Because Abeta depresses synaptic activity, we investigated whether the neurotoxicity of Abeta depends on the expression of NP1, a protein involved in excitatory synapse remodeling that has recently been shown to mediate neuronal death induced by reduction in neuronal activity in mature neurons. We found that treatment of cortical neurons in culture with Abeta produces a marked increase in NP1 protein that precedes apoptotic neurotoxicity. Silencing NP1 gene expression by RNA interference (short hairpin RNA for RNA interference) prevents the loss of synapses, the reduction in neurite outgrowth, and the apoptosis evoked by Abeta. Transgene overexpression of NP1 reproduced these neurotoxic effects of Abeta. Moreover, we found that NP1 was increased in dystrophic neurites of brains from patients with sporadic late-onset Alzheimer's disease. Dual immunohistochemistry for NP1 and tau showed that NP1 colocalizes with tau deposits in dystrophic neurites. Furthermore, NP1 colocalized with SNAP-25 (synaptosomal-associated protein of 25 kDa) in the majority of dystrophic neurites surrounding amyloid deposits. NP1 was also increased in cell processes surrounding amyloid plaques in the cerebral cortex and hippocampus of APP/PS1 (mutant amyloid precursor protein/presenilin 1) transgenic mice. These findings show that NP1 is a key factor for the synapse loss, the neurite damage, and the apoptotic neuronal death evoked by Abeta and indicate that Abeta contributes to the pathology of Alzheimer's disease by regulating NP1 expression.
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