Article citationsMore>>
Oakley, H., Cole, S.L., Logan, S., Maus, E., Shao, P., Craft, J., Guillozet-Bongaarts, A., Ohno, M., Disterhoft, J., Van Eldik, L., Berry, R. and Vassar, R. (2006) Intraneuronal Beta-Amyloid Aggregates, Neurodegeneration, and Neuron Loss in Transgenic Mice with Five Familial Alzheimer’s Disease Mutations: Potential Factors in Amyloid Plaque Fomation. The Journal of Neuroscience, 26, 10129-10140.
http://dx.doi.org/10.1523/JNEUROSCI.1202-06.2006
has been cited by the following article:
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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.
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