Invasion of Hematopoietic Cells into the Brain of Amyloid Precursor Protein Transgenic Mice

Stalder, Anna K.; Ermini, Florian; Bondolfi, Luca; Krenger, Werner; Burbach, Guido J.; Deller, Thomas; Coomaraswamy, Janaky; Staufenbiel, Matthias; Landmann, Régine; Jucker, Mathias

doi:10.1523/jneurosci.2545-05.2005

Cited by 164 publications

(127 citation statements)

References 45 publications

(50 reference statements)

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“…In analogy to our findings in prion disease, microglia engraftment occurred particularly during and after the formation of A␤ deposits and included activation of glial cells around the deposits. In APP23 transgenic AD mice, up to one-quarter of neocortical amyloid plaques were associated with BM-derived cells (Stalder et al, 2005). In conjunction with enhanced infiltration of BMderived cells into the hippocampus after lipopolysaccharide injection, the amount of diffuse A␤ was reduced in APP/PS1 mice (Malm et al, 2005).…”

Section: Microglia Engraftment In Other Neurodegenerative Conditionsmentioning

confidence: 99%

Early and Rapid Engraftment of Bone Marrow-Derived Microglia in Scrapie

Priller

Prinz²,

Heikenwälder³

et al. 2006

J. Neurosci.

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Prion neuroinvasion is accompanied by maximal activation of microglia, the significance of which for pathogenesis is unknown. Here, we used bone marrow (BM) cells expressing GFP (green fluorescent protein) to study the turnover of microglia in mouse scrapie. We found that Ն50% of all brain microglia were replaced by BM-derived cells before clinical disease onset. In terminally sick mice, microglia density increased threefold to fourfold. Hence BM-derived microglia rapidly and efficaciously colonize the brain in scrapie.

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Section: Microglia Engraftment In Other Neurodegenerative Conditionsmentioning

confidence: 99%

Early and Rapid Engraftment of Bone Marrow-Derived Microglia in Scrapie

Priller

Prinz²,

Heikenwälder³

et al. 2006

J. Neurosci.

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“…The perfused brains were immersion-fixed for an additional 24 h in 4% PFA, then cryoprotected in 30% sucrose. Serial 25-m-thick coronal sections were cut using a freezingsliding Microtome and immunohistochemically stained as described previously (44). Polyclonal antibodies NT12 [similar to NT11 (22)] or DW6 (courtesy of D. Walsh) to A␤ were used.…”

Section: Stereotaxic Injection Of Extract Into Different Brainmentioning

confidence: 99%

Induction of cerebral β-amyloidosis: Intracerebral versus systemic Aβ inoculation

Eisele

Bolmont

Heikenwälder

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

259

248

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Despite the importance of the aberrant polymerization of A␤ in the early pathogenic cascade of Alzheimer's disease, little is known about the induction of A␤ aggregation in vivo. Here we show that induction of cerebral ␤-amyloidosis can be achieved in many different brain areas of APP23 transgenic mice through the injection of dilute A␤-containing brain extracts. Once the amyloidogenic process has been exogenously induced, the nature of the induced A␤-deposition is determined by the brain region of the host. Because these observations are reminiscent of a prion-like mechanism, we then investigated whether cerebral ␤-amyloidosis also can be induced by peripheral and systemic inoculations or by the intracerebral implantation of stainless steel wires previously coated with minute amounts of A␤-containing brain extract. Results reveal that oral, intravenous, intraocular, and intranasal inoculations yielded no detectable induction of cerebral ␤-amyloidosis in APP23 transgenic mice. In contrast, transmission of cerebral ␤-amyloidosis through the A␤-contaminated steel wires was demonstrated. Notably, plasma sterilization, but not boiling of the wires before implantation, prevented the induction of ␤-amyloidosis. Our results suggest that minute amounts of A␤-containing brain material in direct contact with the CNS can induce cerebral ␤-amyloidosis, but that systemic cellular mechanisms of prion uptake and transport to the CNS may not apply to A␤.Alzheimer's disease ͉ amyloid ͉ prion ͉ sterilization ͉ transmission

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“…Phagocytic microglia have been detected in the aged APP23 cerebral amyloidosis mouse model in small numbers (58) and in increased abundance in aged Tg2576 mice bearing a CD11c promoter-driven dominant-negative transforming growth factor-␤ receptor type II transgene (18) as well as in the ischemic core after cerebral ischemia in the rat brain (59). However, reactive microglia in both groups of mice reported here had ramified thin and long cell processes and did not appear to be phagocytic based on morphological criteria (amoeboid structure, puffy cytoplasm, few or no processes resembling brain-infiltrating macrophages) (60).…”

Section: Oral Tannic Acid Treatment Mitigates Hyperactivity Andmentioning

confidence: 99%

Tannic Acid Is a Natural β-Secretase Inhibitor That Prevents Cognitive Impairment and Mitigates Alzheimer-like Pathology in Transgenic Mice

Mori

Rezai‐Zadeh

Naoki

et al. 2012

Journal of Biological Chemistry

162

105

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Background: Recent focus has been given to anti-amyloidogenic naturally occurring polyphenols known as flavonoids. Results:The polyphenol tannic acid prevented behavioral impairment and mitigated Alzheimer disease-like pathology. Conclusion: Tannic acid may be prophylactic for Alzheimer disease by inhibiting ␤-secretase activity and mitigating brain pathology. Significance: This nutraceutical approach offers a new class of drug for inhibiting ␤-secretase with few if any side effects.

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Invasion of Hematopoietic Cells into the Brain of Amyloid Precursor Protein Transgenic Mice

Cited by 164 publications

References 45 publications

Early and Rapid Engraftment of Bone Marrow-Derived Microglia in Scrapie

Early and Rapid Engraftment of Bone Marrow-Derived Microglia in Scrapie

Induction of cerebral β-amyloidosis: Intracerebral versus systemic Aβ inoculation

Tannic Acid Is a Natural β-Secretase Inhibitor That Prevents Cognitive Impairment and Mitigates Alzheimer-like Pathology in Transgenic Mice

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