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. Author manuscript; available in PMC: 2016 Sep 1.
Published in final edited form as: Ann Neurol. 2015 Jul 20;78(3):439–453. doi: 10.1002/ana.24454

Figure 7. A biological model for increased Aβ42 exchange and increased irreversible loss.

Figure 7

Faster irreversible loss and exchange are present in amyloidosis (regardless of age, ApoE allele type or cognitive impairment), suggesting that amyloid plaques or associated higher-order Aβ structures (e.g. protofibrils or oligomers) underlie altered Aβ42 kinetics. The FTR may represent irreversible loss due to Aβ42 deposition on plaques, while Aβ42 exchange may represent interactions of newly generated soluble Aβ42 with higher order Aβ structures such as oligomeric forms and amyloid plaques.