Skip to main content
. 2022 Oct 14;13(46):13657–13689. doi: 10.1039/d2sc03932j

Fig. 2. Molecular probe targeting Aβ. (A) NIR fluorescent probes targeting Aβ fibrils (blue and red represent donor and acceptor moieties, respectively). (B) Selective fluorescence response of the CQ probe to Aβ aggregates in comparison with BSA and other amyloid protein aggregates. (C) Fluorescence staining of human brain tissue with CQ and ThT shows selective Aβ aggregate staining by CQ. (D) Immunofluorescence staining of human AD brain tissue shows the selective binding of CQ with Aβ aggregates over tau aggregates as reflected by poor colocalisation with PHF1 tau antibody staining. (E) CQ stain congophilic angiopathy similar to Congo red staining. (B)– (E) Reproduced from ref. 24 with permission from Elsevier, copyright 2017. (F) NIRF imaging of amyloid aggregates in the Tg AD mice model using CRANAD102 at different time interval (min) distinguish AD from WT. Reproduced from ref. 28 with permission from the Royal Society of Chemistry, copyright 2017. (G) Aβ fibril targeting PET probes. (H) PiB PET images of human healthy and AD brains. Reproduced from ref. 33 with permission from the American Neurological Association, copyright 2003.

Fig. 2