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Drug interaction induced memory loss

Miren Ettcheto, Elena Sánchez-López, Yaiza Gómez-Mínguez, Henrry Cabrera, Oriol Busquets, Carlos Beas-Zarate, Maria Luisa García, Eva Carro, Gemma Casadesus, Carme Auladell, Manuel Vázquez Carrera, Jaume Folch, Antoni Camins
There is growing evidence that obesity associated with type 2 diabetes mellitus (T2DM) and aging are risk factors for the development of Alzheimer's disease (AD). However, the molecular mechanisms through which obesity interacts with β-amyloid (Aβ) to promote cognitive decline remains poorly understood. Memantine (MEM), a N-methyl-D-aspartate receptor antagonist, is currently used for the treatment of AD. Nonetheless, few studies have reported its effects on genetic preclinical models of this neurodegenerative disease exacerbated with high-fat diet (HFD)-induced obesity...
February 5, 2018: Molecular Neurobiology
Nathalie T Sanon, Jonathan Gagné, Daniele C Wolf, Soumia Aboulamer, Ciprian M Bosoi, Alexe Simard, Estelle Messiet, Sébastien Desgent, Lionel Carmant
Levetiracetam (LEV), and its newer selective analog brivaracetam (BRV), are two seizure medications that share an innovative mechanism of action targeting the Synaptic Vesicle Protein 2A (SV2A), altering neurotransmitter release and decreasing seizure frequency. Behavioral changes are the most significant adverse effects reported by patients taking LEV. We hypothesize that BRV, the more potent SV2A analog, could exert less behavioral side effects, as it requires lower doses than LEV. Using Kainic Acid (KA)-treated and control rats, we measured adverse behavioral effect profiles of LEV, BRV, or Saline, on social and nonsocial behaviors...
February 2018: Epilepsy & Behavior: E&B
Yuta Hara, Yukio Ago, Atsuki Taruta, Shigeru Hasebe, Haruki Kawase, Wataru Tanabe, Shinji Tsukada, Takanobu Nakazawa, Hitoshi Hashimoto, Toshio Matsuda, Kazuhiro Takuma
RATIONALE: Rodents exposed prenatally to valproic acid (VPA) exhibit autism spectrum disorder (ASD)-like behavioral abnormalities. We recently found that prenatal VPA exposure causes hypofunction of the prefrontal dopaminergic system in mice. This suggests that the dopaminergic system may be a potential pharmacological target for treatment of behavioral abnormalities in ASD patients. OBJECTIVES: In the present study, we examined the effects of antipsychotic drugs, which affect the dopaminergic system, on the social interaction deficits, recognition memory impairment, and reduction in dendritic spine density in the VPA mouse model of ASD...
November 2017: Psychopharmacology
Pradeep Natarajan, Vani Priyadarshini, Dibyabhaba Pradhan, Munikumar Manne, Sandeep Swargam, Hema Kanipakam, Vengamma Bhuma, Umamaheswari Amineni
Glycogen synthase kinase-3β (GSK-3β) is a serine/threonine kinase which has attracted significant attention during recent years in drug design studies. The deregulation of GSK-3β increased the loss of hippocampal neurons by triggering apoptosis-mediating production of neurofibrillary tangles and alleviates memory deficits in Alzheimer's disease (AD). Given its role in the formation of neurofibrillary tangles leading to AD, it has been a major therapeutic target for intervention in AD, hence was targeted in the present study...
October 2016: Journal of Receptor and Signal Transduction Research
Jiang Wu, Bihua Bie, Mohamed Naguib
BACKGROUND: Although neonatal exposure to anesthetic drugs is associated with memory deficiency in rodent models and possibly in pediatric patients, the underlying mechanisms remain elusive. The authors tested their hypothesis that exposure of the developing brain to anesthesia triggers epigenetic modification, involving the enhanced interaction among transcription factors (histone deacetylase 2, methyl-cytosine-phosphate-guanine-binding protein 2, and DNA methyltransferase 1) in Bdnf promoter region(s) that inhibit brain-derived neurotrophic factor (BDNF) expression, resulting in insufficient drive for local translation of synaptic mRNAs...
March 2016: Anesthesiology
I V Zueva, V E Semenov, M A Mukhamedyarov, S V Lushchekina, A D Kharlamova, E O Petukhova, A S Mikhailov, S N Podyachev, L F Saifina, K A Petrov, O A Minnekhanova, V V Zobov, E E Nikolsky, P Masson, V S Reznik
BACKGROUND: Alzheimer's disease (AD) is the major age-related progressive neurodegenerative disorder. The brain of AD patients suffers from loss of cholinergic neurons and decreased number of synapses [1]. AD is caused by an imbalance between Aβ production and clearance, resulting in increased amount of Aβ in various forms [2]. Reduction of Aβ production and increasing clearance of Aβ pathogenic forms are key targets in the development of potential therapeutic agents for AD treatment...
2015: International Journal of Risk & Safety in Medicine
Mauricio O Nava-Mesa, Lydia Jiménez-Díaz, Javier Yajeya, Juan D Navarro-Lopez
Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by cognitive decline, brain atrophy due to neuronal and synapse loss, and formation of two pathological lesions: extracellular amyloid plaques, composed largely of amyloid-beta peptide (Aβ), and neurofibrillary tangles formed by intracellular aggregates of hyperphosphorylated tau protein. Lesions mainly accumulate in brain regions that modulate cognitive functions such as the hippocampus, septum or amygdala. These brain structures have dense reciprocal glutamatergic, cholinergic, and GABAergic connections and their relationships directly affect learning and memory processes, so they have been proposed as highly susceptible regions to suffer damage by Aβ during AD course...
2014: Frontiers in Cellular Neuroscience
Jaspreet Kaur Dhanjal, Sukriti Goyal, Sudhanshu Sharma, Rabia Hamid, Abhinav Grover
Alzheimer's is a neurodegenerative disorder resulting in memory loss and decline in cognitive abilities. Accumulation of extracellular beta amyloidal plaques is one of the major pathology associated with this disease. β-Secretase or BACE-1 performs the initial and rate limiting step of amyloidic pathway in which 37-43 amino acid long peptides are generated which aggregate to form plaques. Inhibition of this enzyme offers a viable prospect to check the growth of these plaques. Numerous efforts have been made in recent years for the generation of BACE-1 inhibitors but many of them failed during the preclinical or clinical trials due to drug related or drug induced toxicity...
January 17, 2014: Biochemical and Biophysical Research Communications
Y Yabuki, Y Ohizumi, A Yokosuka, Y Mimaki, K Fukunaga
Nobiletin, a polymethoxylated flavonoid found in citrus fruit peel, reportedly improves memory impairment in rodent models. Here we report its effect on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced motor and cognitive deficits. Nobiletin administration (50mg/kg i.p.) for 2 consecutive weeks improved motor deficits seen in MPTP-induced Parkinson model mice by 2weeks, an effect that continued until 2weeks after drug withdrawal. Drug treatment promoted similar rescue of MPTP-induced cognitive impairment at equivalent time points...
February 14, 2014: Neuroscience
Puneet Rinwa, Anil Kumar
Prolonged stress causes extensive loss of neurons leading to deficits in cognitive performance. Increasing evidence indicates that accumulation of intercellular messenger, nitric oxide (NO), plays a crucial role in the pathogenesis of memory disorders. American ginseng (AG) is known to show protection in different animal models of neurological diseases; however, its exact mechanism of action is not clearly understood. Therefore, the current study was designed to investigate the interaction of AG against chronic unpredictable stress (CUS)-associated behavioral and biochemical alterations and the probable role of nitrergic pathway in this effect...
February 2014: Naunyn-Schmiedeberg's Archives of Pharmacology
Anil Kumar, Sree Lalitha, Jitendriya Mishra
Epilepsy is a complex neurological disorder manifested by recurrent episodes of convulsive seizures, loss of consciousness, and sensory disturbances. Pentylenetetrazole (PTZ)-induced kindling primarily represents a model of generalized epilepsy. The present study has been undertaken to evaluate the neuroprotective potential of hesperidin and its interaction with nitric oxide modulators against PTZ-induced kindling and associated cognitive dysfunction in mice. The experimental protocol comprised of eleven groups (n=6), where a subconvulsive dose of PTZ (40 mg/kg, i...
October 2013: Epilepsy & Behavior: E&B
Arthur A Nery, Margaret H Magdesian, Cleber A Trujillo, Luciana B Sathler, Maria A Juliano, Luiz Juliano, Henning Ulrich, Sergio T Ferreira
Alzheimer's disease (AD) is characterized by brain accumulation of the neurotoxic amyloid-β peptide (Aβ) and by loss of cholinergic neurons and nicotinic acetylcholine receptors (nAChRs). Recent evidence indicates that memory loss and cognitive decline in AD correlate better with the amount of soluble Aβ than with the extent of amyloid plaque deposits in affected brains. Inhibition of nAChRs by soluble Aβ40 is suggested to contribute to early cholinergic dysfunction in AD. Using phage display screening, we have previously identified a heptapeptide, termed IQ, homologous to most nAChR subtypes, binding with nanomolar affinity to soluble Aβ40 and blocking Aβ-induced inhibition of carbamylcholine-induced currents in PC12 cells expressing α7 nAChRs...
2013: PloS One
Jian Guan, Sam Mathai, Hua-ping Liang, Alistair J Gunn
Ischemic brain damage remains a major cause of disability at all ages. This review examines the efficacy, mode of action and mechanisms of insulin-like growth factor (IGF)-1 and its derivatives in animal models of acute brain injury and neurodegenerative conditions, their potential in pharmaceutical developments. IGF-1 reduces cell loss and improves long-term neurological function in animal models. IGF-1 needs to be given within a few hours of the insult. However, the therapeutic window can be extended by mild hypothermia, likely by delaying apoptosis...
August 2013: Recent Patents on CNS Drug Discovery
Serge H Ahmed, Paul J Kenny
Cocaine addiction is a behavioral disorder defined by behavioral symptoms that set it apart from nondisordered forms of drug use. Here we review evidence in rats (the most frequently used animal model in the field) that it is possible, after extended (but not after limited) access to cocaine for self-administration, to selectively induce some of these behaviors: gradual escalation of cocaine intake, enhanced motivation for the drug despite increased costs (or negative consequences), and increased sensitivity to drug- and stress-primed craving-like behavior...
2011: ILAR Journal
Johnatan Ceccom, Frédéric Coslédan, Hélène Halley, Bernard Francès, Jean Michel Lassalle, Bernard Meunier
Alzheimer's disease (AD) is a neurodegenerative syndrom involving many different biological parameters, including the accumulation of copper metal ions in Aβ amyloid peptides due to a perturbation of copper circulation and homeostasis within the brain. Copper-containing amyloids activated by endogenous reductants are able to generate an oxidative stress that is involved in the toxicity of abnormal amyloids and contribute to the progressive loss of neurons in AD. Since only few drugs are currently available for the treatment of AD, we decided to design small molecules able to interact with copper and we evaluated these drug-candidates with non-transgenic mice, since AD is mainly an aging disease, not related to genetic disorders...
2012: PloS One
Filipe C Matheus, Aderbal S Aguiar, Adalberto A Castro, Jardel G Villarinho, Juliano Ferreira, Cláudia P Figueiredo, Roger Walz, Adair R S Santos, Carla I Tasca, Rui D S Prediger
We have recently demonstrated that rodents treated intranasally with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) suffered impairments in olfactory, cognitive, emotional and motor functions associated with time-dependent disruption of dopaminergic neurotransmission in different brain structures conceivably analogous to those observed during different stages of Parkinson's disease (PD). Agmatine, an endogenous arginine metabolite, has been proposed as a novel neuromodulator that plays protective roles in several models of neuronal cellular damage...
December 1, 2012: Behavioural Brain Research
Jan Drappatz
PURPOSE OF REVIEW: Patients with brain tumors require close attention to medical issues resulting from their disease or its therapy. Effective medical management results in decreased morbidity and mortality and improved quality of life. The most frequent neurology-related issues that arise in these patients include seizures, peritumoral edema, venous thromboembolism, fatigue, and cognitive dysfunction. This article focuses on the most recent findings for the management of the most relevant medical complications among patients with brain tumors...
April 2012: Continuum: Lifelong Learning in Neurology
Rosie Q Li, Andrew R McKinstry, Jason T Moore, Breanna M Caltagarone, Maryellen F Eckenhoff, Roderic G Eckenhoff, Max B Kelz
Hydrogen sulfide (H(2)S) depresses mitochondrial function and thereby metabolic rates in mice, purportedly resulting in a state of "suspended animation." Volatile anesthetics also depress mitochondrial function, an effect that may contribute to their anesthetic properties. In this study, we ask whether H(2)S has general anesthetic properties, and by extension, whether mitochondrial effects underlie the state of anesthesia. We compared loss of righting reflex, electroencephalography, and electromyography in mice exposed to metabolically equipotent concentrations of halothane, isoflurane, sevoflurane, and H(2)S...
June 2012: Journal of Pharmacology and Experimental Therapeutics
Nina N Karpova, Anouchka Pickenhagen, Jesse Lindholm, Ettore Tiraboschi, Natalia Kulesskaya, Arna Agústsdóttir, Hanna Antila, Dina Popova, Yumiko Akamine, Amine Bahi, Regina Sullivan, René Hen, Liam J Drew, Eero Castrén
Antidepressant drugs and psychotherapy combined are more effective in treating mood disorders than either treatment alone, but the neurobiological basis of this interaction is unknown. To investigate how antidepressants influence the response of mood-related systems to behavioral experience, we used a fear-conditioning and extinction paradigm in mice. Combining extinction training with chronic fluoxetine, but neither treatment alone, induced an enduring loss of conditioned fear memory in adult animals. Fluoxetine treatment increased synaptic plasticity, converted the fear memory circuitry to a more immature state, and acted through local brain-derived neurotrophic factor...
December 23, 2011: Science
Rita Guzzi, Mohammad Babavali, Rosa Bartucci, Luigi Sportelli, Mikael Esmann, Derek Marsh
Denaturant-perturbation and pulsed EPR spectroscopy are combined to probe the folding of the membrane-bound Na,K-ATPase active transport system. The Na,K-ATPase enzymes from shark salt gland and pig kidney are covalently spin labelled on cysteine residues that either do not perturb or are essential to hydrolytic activity (Class I and Class II -SH groups, respectively). Urea increases the accessibility of water to the spin-labelled groups and increases their mutual separations, as recorded by D2O interactions from ESEEM spectroscopy and instantaneous spin diffusion from echo-detected EPR spectra, respectively...
June 2011: Biochimica et Biophysica Acta
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