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- A bell-shaped dependence between amyloidosis and GABA accumulation in astrocytes in a mouse model of Alzheimer's disease.
- A new approach for ratiometric in vivo calcium imaging of microglia
- Brain tumor cells interconnect to a functional and resistant network
- Coupled Proliferation and Apoptosis Maintain the Rapid Turnover of Microglia in the Adult Brain
- GABA depolarizes immature neurons and inhibits network activity in the neonatal neocortex in vivo.
- Healthy brain aging: interplay between reactive species, inflammation and energy supply.
- In vivo odorant response properties of migrating adult-born neurons in the mouse olfactory bulb,
- Intracellular calcium stores
- Long-term in vivo single-cell tracking reveals the switch of migration patterns in adult-born juxtaglomerular cells of the mouse
- Longitudinal PET-MRI reveals β-amyloid deposition and rCBF dynamics and connects vascular amyloidosis to quantitative loss of pe
- Impairment of in vivo calcium signaling in amyloid plaque-associated microglia
- Optimized ratiometric calcium sensors for functional in vivo imaging of neurons and T lymphocytes
- Network-wide dysregulation of calcium homeostasis in Alzheimer's disease
- In vivo functional properties of juxtaglomerular neurons in the mouse olfactory bulb
- Microglial calcium signaling in the adult, aged and diseased brain
- Microglial repopulation model reveals a robust homeostatic process for replacing CNS myeloid cells.
- High resolution in vivo imaging of microglia using a versatile non genetically-encoded marker.
- Imaging microcircuit function in healthy and diseased brain
- In vivo functional imaging of the olfactory bulb at single cell resolution
- Novel microglial calcium signal is a rapid sensor of neuronal damage in vivo
- First direct look into the in vivo neuronal activity in the vicinity of Alzheimer-plaques
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A bell-shaped dependence between amyloidosis and GABA accumulation in astrocytes in a mouse model of Alzheimer's disease.
Functioning at the interface between the nervous and immune systems, in the amyloid-depositing brain, astrocytes become hypertrophic and accumulate around senile plaques. Moreover, hippocampal astrocytes upregulate their γ-aminobutyric acid (GABA) content and enhance tonic inhibition, likely causing local circuit imbalance. It remains, however, unclear whether this effect is hippocampus specific and how it is regulated during disease progression. Here, we studied changes in astrocytic morphology and GABA content in the frontal cortex and dentate gyrus of control and amyloid-depositing mice. Healthy aging was accompanied by a transient increase in astrocytic GABA content at middle age and region-specific alterations of soma size. In contrast, amyloid deposition caused a gradual cortex-accentuated increase in soma size. Importantly, our data uncovered a bell-shaped relationship between the mouse age and astrocytic GABA content in both brain regions. Moreover, in mice carrying an Alzheimer's disease-related mutation in presenilin 1, astrocytes accumulated GABA even in the absence of amyloidosis. These data question the proposed inhibition of astrocytic GABA synthesis as a universal strategy for treating network dysfunction in Alzheimer's disease.