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Published on: August 15, 2012
ATG5 (autophagy related 5) in microglia controls hippocampal neurogenesis in Alzheimer disease
Xin Tang1, Ellen Walter1, Eric Wohleb2
1Department of Cancer Biology, University of Cincinnati College Medicine, Cincinnati, OH, USA.
Abstract:
Macroautophagy/autophagy is the intracellular degradation process of cytoplasmic content and damaged organelles. Autophagy is strongly associated with the progression of Alzheimer disease (AD). Microglia are brain-resident macrophages, and recent studies indicate that autophagy in microglia protects neurons from neurodegeneration. Postnatal neurogenesis, the generation of new neurons from adult neural stem cells (NSCs), is impaired in AD patients as well as in AD animal models. However, the extent to which microglial autophagy influences adult NSCs and neurogenesis in AD animal models has not been studied. Here, we showed that conditional knock out (cKO) of Atg5 (autophagy related 5) in microglia inhibited postnatal neurogenesis in the dentate gyrus (DG) of the hippocampus, but not in the subventricular zone (SVZ) of a 5×FAD mouse model. Interestingly, the protection of neurogenesis by Atg5 in microglia was only observed in female AD mice. To confirm the roles of autophagy in microglia for postnatal hippocampal neurogenesis, we generated additional cKO mice to delete autophagy essential genes Rb1cc1 or Atg14 in microglia. However, these rb1cc1 cKO and atg14 cKO mice did not exhibit neurogenesis defects in the context of a female AD mouse model. Last, we used the CSF1R antagonist to deplete ATG5-deficient microglia and this intervention restored neurogenesis in the hippocampus of 5×FAD mice. These results indicate that microglial ATG5 is essential to maintain postnatal hippocampal neurogenesis in a mouse model of AD. Our findings further support the notion that ATG5 in microglia supports NSC health and may prevent neurodegeneration.Abbreviations: 5×FAD: familial Alzheimer disease; Aβ: β-amyloid; AD: Alzheimer disease; AIF1: allograft inflammatory factor 1; ATG: autophagy related; BrdU: 5-bromo-2'-deoxyuridine; CA: Cornu Ammonis; cKO: conditional knock out; CSF1R: colony stimulating factor 1 receptor; Ctrl: control; DCX: doublecortin; DG: dentate gyrus; GFAP: glial fibrillary acidic protein; GZ: granular zone; H&E: hematoxylin and eosin; IF: immunofluorescence; LD: lipid droplet; LDAM: lipid droplets accumulated microglia; LPS: lipopolysaccharides; MAP1LC3B/LC3: microtubule-associated protein 1 light chain 3 beta; NSCs: neural stem cells; RB1CC1: RB1-inducible coiled-coil 1; SOX2: SRY (sex determining region Y)-box 2; SGZ: subgranular zone; SVZ: subventricular zone; WT: wild type.
Insights
Microglial autophagy related 5 (ATG5) is crucial for maintaining neurogenesis in the female Alzheimer disease (AD) mouse hippocampus. Depleting ATG5-deficient microglia restored neurogenesis, highlighting ATG5
Area of Science:
- Neuroscience
- Cellular Biology
- Neurodegeneration Research
Background:
- Autophagy, an intracellular degradation process, is linked to Alzheimer disease (AD) progression.
- Microglial autophagy plays a neuroprotective role, yet its impact on adult neural stem cells (NSCs) in AD remains unclear.
- Postnatal neurogenesis is impaired in AD models, necessitating investigation into factors influencing NSC behavior.
Purpose of the Study:
- To investigate the role of microglial autophagy, specifically autophagy related 5 (ATG5), in regulating postnatal neurogenesis in a mouse model of Alzheimer disease.
- To determine if ATG5 in microglia influences neurogenesis in the hippocampus and subventricular zone (SVZ) of 5×FAD mice.
- To explore the therapeutic potential of targeting microglial autophagy for neurogenesis restoration in AD.
Main Methods:
- Generated conditional knock out (cKO) mice lacking ATG5 specifically in microglia (Atg5 cKO).
- Assessed postnatal neurogenesis in the dentate gyrus (DG) and SVZ of 5×FAD mice using Atg5 cKO models.
- Utilized CSF1R antagonist to deplete ATG5-deficient microglia and evaluated the impact on hippocampal neurogenesis.
Main Results:
- Microglial ATG5 deficiency inhibited postnatal neurogenesis in the DG of female 5×FAD mice but not in the SVZ.
- Deletion of other autophagy genes (Rb1cc1, Atg14) in microglia did not affect neurogenesis in female AD mice.
- Depletion of ATG5-deficient microglia using a CSF1R antagonist restored hippocampal neurogenesis in 5×FAD mice.
Conclusions:
- Microglial ATG5 is essential for maintaining postnatal hippocampal neurogenesis in a female mouse model of Alzheimer disease.
- ATG5 in microglia supports neural stem cell health and may offer a therapeutic target to prevent neurodegeneration.
- The findings underscore a sex-specific role for microglial autophagy in neurogenesis within the context of AD.
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