The neuronal pentraxin Nptx2 regulates complement activity and restrains microglia-mediated synapse loss in neurodegeneration

J Zhou, SD Wade, D Graykowski, MF Xiao… - Science translational …, 2023 - science.org
Complement overactivation mediates microglial synapse elimination in neurological
diseases such as Alzheimer's disease (AD) and frontotemporal dementia (FTD), but how …

[HTML][HTML] Identification of neuronal pentraxins as synaptic binding partners of C1q and the involvement of NP1 in synaptic pruning in adult mice

RÁ Kovács, H Vadászi, É Bulyáki, G Török… - Frontiers in …, 2021 - frontiersin.org
Elements of the immune system particularly that of innate immunity, play important roles
beyond their traditional tasks in host defense, including manifold roles in the nervous …

[HTML][HTML] Neuronal pentraxins as biomarkers of synaptic activity: from physiological functions to pathological changes in neurodegeneration

N Gómez de San José, F Massa… - Journal of Neural …, 2022 - Springer
The diagnosis of neurodegenerative disorders is often challenging due to the lack of
diagnostic tools, comorbidities and shared pathological manifestations. Synaptic dysfunction …

[HTML][HTML] Complement C3 is activated in human AD brain and is required for neurodegeneration in mouse models of amyloidosis and tauopathy

T Wu, B Dejanovic, VD Gandham, A Gogineni… - Cell reports, 2019 - cell.com
Complement pathway overactivation can lead to neuronal damage in various neurological
diseases. Although Alzheimer's disease (AD) is characterized by β-amyloid plaques and tau …

Neuronal pentraxin 2: a synapse-derived CSF biomarker in genetic frontotemporal dementia

EL Van Der Ende, M Xiao, D Xu, JM Poos… - Journal of Neurology …, 2020 - jnnp.bmj.com
Introduction Synapse dysfunction is emerging as an early pathological event in
frontotemporal dementia (FTD), however biomarkers are lacking. We aimed to investigate …

[HTML][HTML] NPTX2 and cognitive dysfunction in Alzheimer's Disease

MF Xiao, D Xu, MT Craig, KA Pelkey, CC Chien, Y Shi… - Elife, 2017 - elifesciences.org
Memory loss in Alzheimer's disease (AD) is attributed to pervasive weakening and loss of
synapses. Here, we present findings supporting a special role for excitatory synapses …

[HTML][HTML] Complement C3aR inactivation attenuates tau pathology and reverses an immune network deregulated in tauopathy models and Alzheimer's disease

A Litvinchuk, YW Wan, DB Swartzlander, F Chen… - Neuron, 2018 - cell.com
Strong evidence implicates the complement pathway as an important contributor to amyloid
pathology in Alzheimer's disease (AD); however, the role of complement in tau modulation …

NPTX2 in cerebrospinal fluid predicts the progression from normal cognition to mild cognitive impairment

A Soldan, S Oh, T Ryu, C Pettigrew, Y Zhu… - Annals of …, 2023 - Wiley Online Library
Objective This study examined whether cerebrospinal fluid (CSF) baseline levels of the
synaptic protein NPTX2 predict time to onset of symptoms of mild cognitive impairment …

[HTML][HTML] NFκB-activated astroglial release of complement C3 compromises neuronal morphology and function associated with Alzheimer's disease

H Lian, L Yang, A Cole, L Sun, ACA Chiang… - Neuron, 2015 - cell.com
Abnormal NFκB activation has been implicated in Alzheimer's disease (AD). However, the
signaling pathways governing NFκB regulation and function in the brain are poorly …

Neuronal pentraxin 1 contributes to the neuronal damage evoked by amyloid-β and is overexpressed in dystrophic neurites in Alzheimer's brain

MA Abad, M Enguita… - Journal of …, 2006 - Soc Neuroscience
Accumulation of amyloid-β (Aβ) 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 …