Alzheimer's Disease & Dementia

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Ayat Kaeidi, J Alzheimers Dis Parkinsonism 2017, 7:6(Suppl) conferenceseries.com DOI: 10.4172/2161-0460-C1-034 9th International Conference on ALZHEIMER’S DISEASE & DEMENTIA October 16-18, 2017 | Rome, Italy Ampakine Farampator (CX691) improves cognitive impairment and hippocampus BDNF levels in a rat model of Aβ1-42-induced Alzheimer's disease Ayat Kaeidi Rafsanjan University of Medical Sciences, Iran n emerging body of data suggests that dysfunction of the glutamatergic system and AMPA receptors has been implicated Ain Alzheimer’s disease (AD). Because AMPA receptor plays a critical role in the regulation of hippocampus synaptic plasticity, the positive modulation of this receptors may rescue learning and memory deficits in AD. In the present study, by using the Morris water maze paradigm, we explored the pro-cognitive effect of Farampator, a specific positive allosteric modulator of the AMPA-type glutamate receptors in rat model of AD produced by injection of amyloid-beta1-42 (Aβ1-42) in to the hippocampus. Furthermore, we investigated the effects of Farampator on brain derived neurotrophic factor (BDNF) protein expression in the hippocampus tissue. Results show that intrahippocampal injection of Aβ1-42 caused learning and memory deficits in rats subjected to the Morris water maze and decreased BDNF expression in the hippocampus. Also we found that treatment with farampator for 10 days (0.3 mg/kg, twice a day) improved the performance of Alzheimeric rats in Morris water navigation task with increased level of BDNF protein. Altogether, our data suggest that Farampator ameliorate Aβ1-42-induced learning deficits, at least part, via up-regulation of BDNF protein in the hippocampus. The results of this investigation may shed light on a possible therapeutic approach to treating and control the progression of AD. Biography Ayat Kaeidi has started his PhD at the age of 32 years from Rafsanjan University of Medical Sciences. He has published more than 12 papers in reputed journals. [email protected] Notes: J Alzheimers Dis Parkinsonism, an open access journal Volume 7, Issue 6 (Suppl) ISSN: 2161-0460 Dementia 2017 October 16-18, 2017 Page 67.

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Effects of Chronic Systemic Low-Impact Ampakine Treatment On
Biomedicine & Pharmacotherapy 105 (2018) 540–544 Contents lists available at ScienceDirect Biomedicine & Pharmacotherapy journal homepage: www.elsevier.com/locate/biopha Effects of chronic systemic low-impact ampakine treatment on neurotrophin T expression in rat brain ⁎ Daniel P. Radin , Steven Johnson, Richard Purcell, Arnold S. Lippa RespireRx Pharmaceuticals, Inc., 126 Valley Road, Glen Rock, NJ, 07452, United States ARTICLE INFO ABSTRACT Keywords: Neurotrophin dysregulation has been implicated in a large number of neurodegenerative and neuropsychiatric Ampakine diseases. Unfortunately, neurotrophins cannot cross the blood brain barrier thus, novel means of up regulating BDNF their expression are greatly needed. It has been demonstrated previously that neurotrophins are up regulated in Cognitive enhancement response to increases in brain activity. Therefore, molecules that act as cognitive enhancers may provide a LTP clinical means of up regulating neurotrophin expression. Ampakines are a class of molecules that act as positive Neurotrophin allosteric modulators of AMPA-type glutamate receptors. Currently, they are being developed to prevent opioid- NGF induced respiratory depression without sacrificing the analgesic properties of the opioids. In addition, these molecules increase neuronal activity and have been shown to restore age-related deficits in LTP in aged rats. In the current study, we examined whether two different ampakines could increase levels of BDNF and NGF at doses that are active in behavioral measures of cognition. Results demonstrate that ampakines CX516 and CX691 induce differential increases in neurotrophins across several brain regions. Notable increases in NGF were ob- served in the dentate gyrus and piriform cortex while notable BDNF increases were observed in basolateral and lateral nuclei of the amygdala.
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