Alzheimer’s disease (AD) is a progressive neurodegenerative disorder and the fourth leading
cause of death in the United States and most common cause of adult-onset dementia. The major
hallmarks of AD are the formation of senile amyloid plaques made of beta amyloid and neurofibrillary
tangles (NFT) which are primarily composed of phosphorylated tau protein. Although numerous
agents have been considered as providing protection against AD, identification of potential agents
with neuroprotective ability is limited. Thioflavin T has been used in the past to stain amyloid beta
plaques in brain. In this study, Thioflavin T (ThT) and vehicle (infant formula) were administered
orally by gavage to transgenic (B6C3 APP PS1; AD-Tg) mice beginning at 4 months age and continuing until sacrifice at
9 months of age at 40mg/kg dose. The number of amyloid plaques was reduced dramatically by ThT treatment in both
male and female transgenic mice compared to those in control mice. Additionally, GFAP and Amylo-Glo labeling suggest
that astrocytic hypertrophy is minimized in ThT-treated animals. Similarly, CD68 labeling, which detects activated microglia,
along with Amylo-Glo labeling, suggests that microglial activation is significantly less in ThT-treated mice. Both
Aβ-40 and Aβ-42 concentrations in blood rose significantly in the ThT-treated animals suggesting that ThT may inhibit
the deposition, degradation, and/or clearance of Aβ plaques in brain.
Keywords: AD, Amylo-Glo, astrocytes, CD68, GFAP, microglia, neuroprotection, thioflavin T.
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