Increased T Cell Recruitment to the CNS after Amyloid β_1–42Immunization in Alzheimer's Mice Overproducing Transforming Growth Factor-β1

IFN‐γ enhances neurogenesis in wild‐type mice and in a mouse model of Alzheimer's disease

“…This A␤-induced glial activation becomes chronic with time and promotes further neuronal damage. In the AD brain, glial activation includes but is not limited to excess production of IL-1␤, TNF-␣, IL-6, and TGF-␤, all of which can suppress neurogenesis (11)(12)(13)(14)42). Indeed, we found decreased neurogenesis and enhanced oligodendrogenesis in APP Tg mice, which may be primarily due to the role of IL-6 in promoting NPC differentiation to oligodendrocytes (14,43).…”

IFN‐γ enhances neurogenesis in wild‐type mice and in a mouse model of Alzheimer's disease

“…This A␤-induced glial activation becomes chronic with time and promotes further neuronal damage. In the AD brain, glial activation includes but is not limited to excess production of IL-1␤, TNF-␣, IL-6, and TGF-␤, all of which can suppress neurogenesis (11)(12)(13)(14)42). Indeed, we found decreased neurogenesis and enhanced oligodendrogenesis in APP Tg mice, which may be primarily due to the role of IL-6 in promoting NPC differentiation to oligodendrocytes (14,43).…”

Whole‐body senescent cell clearance alleviates age‐related brain inflammation and cognitive impairment in mice

“…It was recently reported that T cells infiltrate into the periventricular brain regions of old mice (Dulken et al, 2019; Ritzel et al, 2016). This process has been linked to brain inflammation and neurodegeneration (Buckwalter et al, 2006; Dulken et al, 2019). As the SASP has been shown to recruit immune cells, including T cells (Kang et al, 2011; Sagiv & Krizhanovsky, 2013), we hypothesized that targeting senescent cells could impact the number of infiltrating immune cells in the brains of aged mice.…”

Comprehensive transcriptional profiling of prion infection in mouse models reveals networks of responsive genes

“…Indeed, TGF-beta1 is largely produced in astrocytes and microglia but can be expressed in neurons. Over expression of TGF-beta1 in astrocytes protects adult mice against neurodegeneration during acute, excitotoxic and chronic injury [ 16 ], its loss leads to increased neuronal cell death and gliosis [ 17 , 18 ]. Its role during prion induced neurodegeneration is likely to be to suppress inflammation in the brain that could exacerbate the course of the disease.…”

IFN‐γ enhances neurogenesis in wild‐type mice and in a mouse model of Alzheimer's disease

“…This A␤-induced glial activation becomes chronic with time and promotes further neuronal damage. In the AD brain, glial activation includes but is not limited to excess production of IL-1␤, TNF-␣, IL-6, and TGF-␤, all of which can suppress neurogenesis (11)(12)(13)(14)42). Indeed, we found decreased neurogenesis and enhanced oligodendrogenesis in APP Tg mice, which may be primarily due to the role of IL-6 in promoting NPC differentiation to oligodendrocytes (14,43).…”

Whole‐body senescent cell clearance alleviates age‐related brain inflammation and cognitive impairment in mice

“…It was recently reported that T cells infiltrate into the periventricular brain regions of old mice (Dulken et al, 2019; Ritzel et al, 2016). This process has been linked to brain inflammation and neurodegeneration (Buckwalter et al, 2006; Dulken et al, 2019). As the SASP has been shown to recruit immune cells, including T cells (Kang et al, 2011; Sagiv & Krizhanovsky, 2013), we hypothesized that targeting senescent cells could impact the number of infiltrating immune cells in the brains of aged mice.…”

Comprehensive transcriptional profiling of prion infection in mouse models reveals networks of responsive genes

“…Indeed, TGF-beta1 is largely produced in astrocytes and microglia but can be expressed in neurons. Over expression of TGF-beta1 in astrocytes protects adult mice against neurodegeneration during acute, excitotoxic and chronic injury [ 16 ], its loss leads to increased neuronal cell death and gliosis [ 17 , 18 ]. Its role during prion induced neurodegeneration is likely to be to suppress inflammation in the brain that could exacerbate the course of the disease.…”

IFN‐γ enhances neurogenesis in wild‐type mice and in a mouse model of Alzheimer's disease

“…This A␤-induced glial activation becomes chronic with time and promotes further neuronal damage. In the AD brain, glial activation includes but is not limited to excess production of IL-1␤, TNF-␣, IL-6, and TGF-␤, all of which can suppress neurogenesis (11)(12)(13)(14)42). Indeed, we found decreased neurogenesis and enhanced oligodendrogenesis in APP Tg mice, which may be primarily due to the role of IL-6 in promoting NPC differentiation to oligodendrocytes (14,43).…”

Whole‐body senescent cell clearance alleviates age‐related brain inflammation and cognitive impairment in mice

“…It was recently reported that T cells infiltrate into the periventricular brain regions of old mice (Dulken et al, 2019; Ritzel et al, 2016). This process has been linked to brain inflammation and neurodegeneration (Buckwalter et al, 2006; Dulken et al, 2019). As the SASP has been shown to recruit immune cells, including T cells (Kang et al, 2011; Sagiv & Krizhanovsky, 2013), we hypothesized that targeting senescent cells could impact the number of infiltrating immune cells in the brains of aged mice.…”

Comprehensive transcriptional profiling of prion infection in mouse models reveals networks of responsive genes

“…Indeed, TGF-beta1 is largely produced in astrocytes and microglia but can be expressed in neurons. Over expression of TGF-beta1 in astrocytes protects adult mice against neurodegeneration during acute, excitotoxic and chronic injury [ 16 ], its loss leads to increased neuronal cell death and gliosis [ 17 , 18 ]. Its role during prion induced neurodegeneration is likely to be to suppress inflammation in the brain that could exacerbate the course of the disease.…”