Affiliations: [a] Department of Neurology, Texas A&M University System HSC College of Medicine, Temple, TX, USA | [b] Department of Research & Education, Scott and White Clinic, Texas A&M University System HSC College of Medicine, Temple, TX, USA | [c] Department of Internal Medicine, Texas A&M University System HSC College of Medicine, Temple, TX, USA | [d] Department of Psychiatry and Behavioral Science, Texas A&M University System HSC College of Medicine, Temple, TX, USA | [e] Central Texas Veterans Health Care System Neuropsychiatry Research Program, Temple, TX, USA | [f] Division of Pharmacology & Toxicology, Department of Pharmacal Sciences, Auburn University, Auburn, AL, USA
Correspondence:
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Corresponding author: Bala V. Manyam, M.D., Department of Neurology, Scott & White Clinic/Texas A&M University, 2401 South 31st street, Temple, TX 76508, USA. Tel.: +1 813 792 9524; Fax: +1 254 724 5692; E-mail: [email protected].
Abstract: PSAPP mice expressing the “Swedish” amyloid precursor protein and M146L presenilin-1 mutations are a well-characterized model for spontaneous amyloid plaque formation. Bacopa monniera has a long history of use in India as an anti-aging and memory-enhancing ethnobotanical therapy. To evaluate the effect of Bacopa monniera extract (BME) on amyloid (Aβ) pathology in PSAPP mice, two doses of BME (40 or 160 mg/kg/day) were administered starting at 2 months of age for either 2 or 8 months. Our present data suggests that BME lowers Aβ 1-40 and 1-42 levels in cortex by as much as 60%, and reverses Y-maze performance and open field hyperlocomotion behavioral changes present in PSAPP mice. The areas encompassed by Congo Red-positive fibrillar amyloid deposits, however, were not altered by BME treatment. The data suggest that BME has potential application in Alzheimer's disease therapeutics.
