Skip to main content
. Author manuscript; available in PMC: 2017 Mar 27.
Published in final edited form as: Brain. 2014 Sep 10;137(Pt 11):2909–2915. doi: 10.1093/brain/awu255

Figure 2.

Figure 2

Human CSF does not induce cerebral β-amyloidosis. The soluble fraction of an Alzheimer’s disease brain extract (supernatant, see Fig. 1) and undiluted human CSF were injected into young, pre-depositing 3- to 4-month-old APP23 transgenic mice (2.5 μl bilaterally). Brains were immunohistochemically analysed for amyloid-β deposition after a 6–8 month incubation period (Supplementary Table 1). (A) The supernatant (SN) fraction of an Alzheimer’s disease patient induced the expected amyloid-β deposition (see Fig. 1A). (B and C) Neither CSF from Alzheimer’s disease patients (shown is A023) nor control subjects (shown is A009) revealed any amyloid-β deposition. CSF from eight Alzheimer’s disease patients and six control subjects was tested in 2–10 mice per CSF sample. Two CSF samples were tested both fresh and frozen (for details see Supplementary Table 1). The total number of animals with induced amyloid-β deposition/total number of animals tested is indicated. Scale bar = 200 μm. AD = Alzheimer’s disease.