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Oral Administration of Thioflavin T Prevents Beta Amyloid Plaque Formation in Double Transgenic AD Mice.
Curr Alzheimer Res 2015; 12(9):837-46CA

Abstract

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 40 mg/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.

Authors+Show Affiliations

National Center for Toxicological Research/FDA, 3900 NCTR Road, HFT-132, Jefferson, AR-72079, USA. sumit.sarkar@fda.hhs.gov.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

26510980

Citation

Sarkar, Sumit, et al. "Oral Administration of Thioflavin T Prevents Beta Amyloid Plaque Formation in Double Transgenic AD Mice." Current Alzheimer Research, vol. 12, no. 9, 2015, pp. 837-46.
Sarkar S, Raymick J, Ray B, et al. Oral Administration of Thioflavin T Prevents Beta Amyloid Plaque Formation in Double Transgenic AD Mice. Curr Alzheimer Res. 2015;12(9):837-46.
Sarkar, S., Raymick, J., Ray, B., Lahiri, D. K., Paule, M. G., & Schmued, L. (2015). Oral Administration of Thioflavin T Prevents Beta Amyloid Plaque Formation in Double Transgenic AD Mice. Current Alzheimer Research, 12(9), pp. 837-46.
Sarkar S, et al. Oral Administration of Thioflavin T Prevents Beta Amyloid Plaque Formation in Double Transgenic AD Mice. Curr Alzheimer Res. 2015;12(9):837-46. PubMed PMID: 26510980.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Oral Administration of Thioflavin T Prevents Beta Amyloid Plaque Formation in Double Transgenic AD Mice. AU - Sarkar,Sumit, AU - Raymick,James, AU - Ray,Balmiki, AU - Lahiri,Debomoy K, AU - Paule,Merle G, AU - Schmued,Larry, PY - 2015/02/02/received PY - 2015/04/06/revised PY - 2015/04/27/accepted PY - 2015/10/30/entrez PY - 2015/10/30/pubmed PY - 2016/8/5/medline SP - 837 EP - 46 JF - Current Alzheimer research JO - Curr Alzheimer Res VL - 12 IS - 9 N2 - 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 40 mg/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. SN - 1875-5828 UR - https://www.unboundmedicine.com/medline/citation/26510980/Oral_Administration_of_Thioflavin_T_Prevents_Beta_Amyloid_Plaque_Formation_in_Double_Transgenic_AD_Mice_ L2 - http://www.eurekaselect.com/135880/article DB - PRIME DP - Unbound Medicine ER -