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. Author manuscript; available in PMC: 2022 Apr 16.
Published in final edited form as: Drug Discov Today. 2018 May 7;23(6):1305–1311. doi: 10.1016/j.drudis.2018.05.009

FIGURE 2.

FIGURE 2

Adiponectin (APN) paradox in Alzheimer’s disease (AD), (a) Immunofluorescence of APN and tau. In autopsied AD brains, but not in controls, immunoreactivity of APN converged intracellularly with that of tau (PHF). (b) By contrast, a cellular study showed that APN was protective against oxidative stress-induced cytotoxicity in Aβ neurotoxicity in SH-SY5Y neuroblastoma cells expressing the Swedish mutant of amyloid precursor protein (APP). (c) Immunofluorescence of APN and phosphor-αS. In autopsied brains from patients with dementia with Lewy bodies (DLB), immunoreactivity of APN converged with that of phosphor αS in Lewy bodies, (d) Representative immunohistochemical images of the cortex stained with anti-pαS. αS transgenic mice and their nontransgenic littermates were treated with globular APN or PBS for 3 months, followed by various assessments. Insets are shown at a higher magnification for the cortex. Reproduced from Refs [26] (a), [36] (b), and [27] (c,d).