E.Author ContributionsConceived and designed the experiments: FH. Performed the experiments

E.Author ContributionsConceived and designed the experiments: FH. Performed the experiments: FH. Analyzed the data: SY. Contributed reagents/materials/analysis tools: YXS. Wrote the paper: FH.
Neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD) and Parkinson’s disease (PD), are incurable and debilitating conditions that result in the progressive degeneration and death of neurons. Despite numerous attempts to identify a treatment strategy for these diseases, there have been no effective therapies to date. Neurotrophic factors (NTFs), such as nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF) and glial cell-line derived neurotrophic factor (GDNF), play pivotal roles in neuronal development and survival and exhibit therapeutic potential in animal models of neurodegenerative diseases [1]. NGF and BDNF also show neurotrophic actions on the cholinergic neurons of the basal forebrain, protecting them against axotomy-induced neurodegeneration and age-related atrophy [2,3]. Local delivery of NGF to the cholinergic basal forebrain of non-human primates can arrest and even reverse the degeneration of cholinergic neurons that contribute to cognitive decline in AD [4]. GDNF also has robust effects on the survival of dopaminergic neurons in PD [5,6]. In addition to NTFs, some growth factors, such as vascular endothelial growth factor (VEGF), insulin-like growth factor 1 (IGF1) and hepatocyte growth factor (HGF), have also been shownto exert neuroprotective effects in animal models of ALS [7,8,9]. Although these neurotrophic factors and growth factors may have therapeutic potential as neuroprotective factors, most studies have examined these effects using recombinant protein administration and transgenic expression or virus vector-mediated gene transfer. Therefore, it is important to determine if any endogenous factors exert neuroprotective Title Loaded From File activities in an injured or diseased nervous system. B cell activating factor (BAFF) is a member of the tumor necrosis factor (TNF) family and is expressed on the surface of monocytes, dendritic cells, neutrophils, stromal cells, activated T cells, malignant B cells and epithelial cells [10]. Cleaved BAFF binds to three different receptors, notably BAFF receptor (BAFFR), transmembrane activator and calcium modulator and cyclophilin ligand interactor (TACI) and B cell maturation protein (BCMA), that are expressed differentially at various stages of B cell ontogeny [11]. The ligation of Of AmpliTaq Gold DNA Polymerase (Applied Biosystems). PCR was conducted under BAFF-R by BAFF delivers the potent signals for the survival of B lymphocytes leading to effective humoral immune responses. BAFF transgenic mice develop B cell hyperplasia from the T2 B cell stage, whereas BAFF- and BAFFR eficient mice show impaired B cell maturation beyond the T1 stage, decreased immunoglobulin levels, and decreased T cell-Neuroprotection by B Cell Activating Factor (BAFF)dependent and -independent immune responses [12]. These previous findings suggest that, unlike other members of the TNF family, BAFF has its biological activity to a limited repertoire of cell lineages such as B cells. Despite the indispensible function of BAFF in 23977191 B cell development, a recent study demonstrated BAFF expression in the normal central nervous system (CNS) and some pathogenic lesions of CNS diseases including multiple sclerosis (MS) and primary CNS lymphoma, however it is uncertain whether BAFF contributes to neuronal activity or the disease progression. In the present work.E.Author ContributionsConceived and designed the experiments: FH. Performed the experiments: FH. Analyzed the data: SY. Contributed reagents/materials/analysis tools: YXS. Wrote the paper: FH.
Neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD) and Parkinson’s disease (PD), are incurable and debilitating conditions that result in the progressive degeneration and death of neurons. Despite numerous attempts to identify a treatment strategy for these diseases, there have been no effective therapies to date. Neurotrophic factors (NTFs), such as nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF) and glial cell-line derived neurotrophic factor (GDNF), play pivotal roles in neuronal development and survival and exhibit therapeutic potential in animal models of neurodegenerative diseases [1]. NGF and BDNF also show neurotrophic actions on the cholinergic neurons of the basal forebrain, protecting them against axotomy-induced neurodegeneration and age-related atrophy [2,3]. Local delivery of NGF to the cholinergic basal forebrain of non-human primates can arrest and even reverse the degeneration of cholinergic neurons that contribute to cognitive decline in AD [4]. GDNF also has robust effects on the survival of dopaminergic neurons in PD [5,6]. In addition to NTFs, some growth factors, such as vascular endothelial growth factor (VEGF), insulin-like growth factor 1 (IGF1) and hepatocyte growth factor (HGF), have also been shownto exert neuroprotective effects in animal models of ALS [7,8,9]. Although these neurotrophic factors and growth factors may have therapeutic potential as neuroprotective factors, most studies have examined these effects using recombinant protein administration and transgenic expression or virus vector-mediated gene transfer. Therefore, it is important to determine if any endogenous factors exert neuroprotective activities in an injured or diseased nervous system. B cell activating factor (BAFF) is a member of the tumor necrosis factor (TNF) family and is expressed on the surface of monocytes, dendritic cells, neutrophils, stromal cells, activated T cells, malignant B cells and epithelial cells [10]. Cleaved BAFF binds to three different receptors, notably BAFF receptor (BAFFR), transmembrane activator and calcium modulator and cyclophilin ligand interactor (TACI) and B cell maturation protein (BCMA), that are expressed differentially at various stages of B cell ontogeny [11]. The ligation of BAFF-R by BAFF delivers the potent signals for the survival of B lymphocytes leading to effective humoral immune responses. BAFF transgenic mice develop B cell hyperplasia from the T2 B cell stage, whereas BAFF- and BAFFR eficient mice show impaired B cell maturation beyond the T1 stage, decreased immunoglobulin levels, and decreased T cell-Neuroprotection by B Cell Activating Factor (BAFF)dependent and -independent immune responses [12]. These previous findings suggest that, unlike other members of the TNF family, BAFF has its biological activity to a limited repertoire of cell lineages such as B cells. Despite the indispensible function of BAFF in 23977191 B cell development, a recent study demonstrated BAFF expression in the normal central nervous system (CNS) and some pathogenic lesions of CNS diseases including multiple sclerosis (MS) and primary CNS lymphoma, however it is uncertain whether BAFF contributes to neuronal activity or the disease progression. In the present work.