Meeting Abstract
Plaques in the brain formed through the accumulation of amyloid beta (Aβ) peptide are a characteristic symptom of Alzheimer’s disease (AD). Aβ originates within the brain and peripheral tissues and contributes to pathologies in each. The blood-brain barrier (BBB) regulates Aβ influx from peripheral sources, and the membrane proteins responsible for Aβ clearance lose their function as AD progresses. We examined the testes which have a blood-tissue barrier (BTB) that is similar to the BBB and are thus potentially susceptible to similar Aβ accumulation and subsequent cell damage. We expected that the process of spermatogenesis in transgenic (Tg) APPswe/PS1dE9 mice would be altered relative to non-transgenic (non-Tg) mice and that human Aβ would be present in testicular tissue of Tg but not non-Tg mice. Testes from adult male mice were stained with H&E, and cells from each stage of spermatogenesis were recorded. We then used immunohistochemistry to determine the cellular location of Aβ-immunoreactivity (ir) in testicular tissue. We found that spermatogenesis does not differ between genotypes despite the presence of Aβ-ir within the seminiferous tubules of Tg mice. Aβ-ir was blocked by preadsorption with human Aβ 1-40 but not mouse Aβ 1-40. Current work is focused on analytical determination of the Aβ form present in the testes of Tg mice and its potential colocalization with Sertoli cells. Since the testes possess a BTB similar to the BBB, this research will elucidate details about the integrity of the body’s BTBs in AD. Furthermore, our research will add to our understanding of Alzheimer’s pathology in peripheral tissues. Partially funded by NIH 1R15AG048447.
