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Borchelt, D.R., Ratovitski, T., van Lare, J., Lee, M.K., Gonzales, V., Jenkins, N.A., Copeland, N.G., Price, D.L. and Sisodia, S. (1997) Accelerated Amyloid Deposition in the Brains of Transgenic mice Coexpressing Mutant Presenilin 1 and Amyloid Precursor Proteins. Neuron, 19, 939-945.
http://dx.doi.org/10.1016/S0896-6273(00)80974-5

has been cited by the following article:

• TITLE: Reserpine Improves Working Memory

  AUTHORS: Raghuraman Vasantharaja, Ajeet Kumar, Ashok Kumar, Jamuna R. Subramaniam

  KEYWORDS: Alzheimer’s Disease, Amyloid-β-Aβ, Reserpine, Cognitive Deficits, Transgenic Mice, Working Memory

  JOURNAL NAME: Journal of Behavioral and Brain Science, Vol.6 No.3, March 11, 2016

  ABSTRACT: Despite exhaustive search, no drug is in sight for AD. Earlier, we reported that reserpine, an antihypertensive and antipsychotic drug, ameliorates Amyloid beta (Aβ-AD causing peptide) toxicity and confers several positive enhancements in the C. elegans model system. Here, we evaluate whether reserpine can provide protection against working memory and against AD in the mouse model. Reserpine (0.08 mg) was administered orally on alternate days to the non-Tg and accelerated Aβ deposition (at 2 months of age)and cognitive deficit (4 months of age) developing 5XFAD AD Tg mouse model expressing mutant human APP (3 familial mutations) and human Presenilin1(2 familial mutations) in the neurons, and follow their working memory for 2 months using the spontaneous Y-maze alteration behavioral paradigm. Reserpine enhanced working memory in non-Tg mice and improved the cognitive deficit in the 5XFAD AD Tg mice. Hence, reserpine can be considered for a detailed evaluation in the 3X Tg AD mouse model and a pilot study in AD patients.