TY - JOUR AU - Aquino, Ruth AU - de Concini, Vidian AU - Dhenain, Marc AU - Lam, Suzanne AU - Gosset, David AU - Baquedano, Laura AU - Forero, Manuel G. G. AU - Menuet, Arnaud AU - Baril, Patrick AU - Pichon, Chantal TI - Intrahippocampal Inoculation of A beta(1-42) Peptide in Rat as a Model of Alzheimer's Disease Identified MicroRNA-146a-5p as Blood Marker with Anti-Inflammatory Function in Astrocyte Cells JF - CELLS J2 - CELLS-BASEL VL - 12 PY - 2023 IS - 5 PG - 24 SN - 2073-4409 DO - 10.3390/cells12050694 UR - https://m2.mtmt.hu/api/publication/33894152 ID - 33894152 AB - Circulating microRNAs (miRNAs) have aroused a lot of interest as reliable blood diagnostic biomarkers of Alzheimer's disease (AD). Here, we investigated the panel of expressed blood miRNAs in response to aggregated A beta(1-42) peptides infused in the hippocampus of adult rats to mimic events of the early onset of non-familial AD disorder. A beta(1-42) peptides in the hippocampus led to cognitive impairments associated with an astrogliosis and downregulation of circulating miRNA-146a-5p, -29a-3p, -29c-3p, -125b-5p, and-191-5p. We established the kinetics of expression of selected miRNAs and found differences with those detected in the APP(swe)/PS1(dE9) transgenic mouse model. Of note, miRNA-146a-5p was exclusively dysregulated in the A beta-induced AD model. The treatment of primary astrocytes with A beta(1-42) peptides led to miRNA-146a-5p upregulation though the activation of the NF-kappa B signaling pathway, which in turn downregulated IRAK-1 but not TRAF-6 expression. As a consequence, no induction of IL-1 beta, IL-6, or TNF-alpha was detected. Astrocytes treated with a miRNA-146-5p inhibitor rescued IRAK-1 and changed TRAF-6 steady-state levels that correlated with the induction of IL-6, IL-1 beta, and CXCL1 production, indicating that miRNA-146a-5p operates anti-inflammatory functions through a NF-kappa B pathway negative feedback loop. Overall, we report a panel of circulating miRNAs that correlated with A beta(1-42) peptides' presence in the hippocampus and provide mechanistic insights into miRNA-146a-5p biological function in the development of the early stage of sporadic AD. LA - English DB - MTMT ER - TY - JOUR AU - Forero, Manuel G. AU - Hernandez, Natalia C. AU - Morera, Cristian M. AU - Aguilar, Luis A. AU - Aquino, Ruth AU - Baquedano, Laura E. TI - A new automatic method for tracking rats in the Morris water maze JF - HELIYON J2 - HELIYON VL - 9 PY - 2023 IS - 7 PG - 11 SN - 2405-8440 DO - 10.1016/j.heliyon.2023.e18367 UR - https://m2.mtmt.hu/api/publication/34282529 ID - 34282529 AB - Morris water maze (MWM) test is widely used to evaluate the learning and memory deficits in rodents. Image processing and pattern recognition can be used to analyse videos and recognize automatically the tracking in MWM. There are several commercial and free access software that allows analyzing the behavioral tasks although they also have limitations such as automation, cost, user intervention among other things. The aim of this paper was to develop a new image processing technique to automatically analyse the track of the rat in the MWM, which we called RatsTrack. The MWM test was performed with an animal model for Alzheimer, and the videos were recorded to measure the distance, time, and speed. The segmentation method based on the projection of the video frames was made for pool identification, eliminating the rat, while conserving the shape of the pool. Then, the Hough transformation was used to recognize the position and radius of the pool. Finally, the frame in which the rat is released into the pool was established automatically using mathematical morphology techniques and added as a plugin on free access ImageJ software. The new image processing technique, RatsTrack, successfully detected and located the pool and rat without user intervention, significantly decreasing operational time and providing results for distance, time, speed, and acceleration parameters of the MWM test. Alzheimer's rats compared with the control group presented significant data measured with the RatsTrack. RatsTrack is a plugin of ImageJ software and will be made freely available for public use. LA - English DB - MTMT ER - TY - JOUR AU - Lorden, Gema AU - Wozniak, Jacob M. AU - Dore, Kim AU - Dozier, Lara E. AU - Cates-Gatto, Chelsea AU - Patrick, Gentry N. AU - Gonzalez, David J. AU - Roberts, Amanda J. AU - Tanzi, Rudolph E. AU - Newton, Alexandra C. TI - Enhanced activity of Alzheimer disease-associated variant of protein kinase C alpha drives cognitive decline in a mouse model JF - NATURE COMMUNICATIONS J2 - NAT COMMUN VL - 13 PY - 2022 IS - 1 PG - 16 SN - 2041-1723 DO - 10.1038/s41467-022-34679-7 UR - https://m2.mtmt.hu/api/publication/33894153 ID - 33894153 AB - Exquisitely tuned activity of protein kinase C (PKC) isozymes is essential to maintaining cellular homeostasis. Whereas loss-of-function mutations are generally associated with cancer, gain-of-function variants in one isozyme, PKC alpha, are associated with Alzheimer's disease (AD). Here we show that the enhanced activity of one variant, PKC alpha M489V, is sufficient to rewire the brain phosphoproteome, drive synaptic degeneration, and impair cognition in a mouse model. This variant causes a modest 30% increase in catalytic activity without altering on/off activation dynamics or stability, underscoring that enhanced catalytic activity is sufficient to drive the biochemical, cellular, and ultimately cognitive effects observed. Analysis of hippocampal neurons from PKC alpha M489V mice reveals enhanced amyloid-beta-induced synaptic depression and reduced spine density compared to wild-type mice. Behavioral studies reveal that this mutation alone is sufficient to impair cognition, and, when coupled to a mouse model of AD, further accelerates cognitive decline. The druggability of protein kinases positions PKC alpha as a promising therapeutic target in AD.Mutations that enhance the activity of protein kinase C alpha (PKC alpha) are associated with Alzheimer's Disease. Here, the authors report that the enhanced activity of one variant, PKC alpha M489V, is sufficient to rewire the brain phosphoproteome, drive synaptic degeneration, and impair cognition in a mouse model. LA - English DB - MTMT ER - TY - JOUR AU - Davis, Nicola AU - Mota, Bibiana C. AU - Stead, Larissa AU - Palmer, Emily O. C. AU - Lombardero, Laura AU - Rodriguez-Puertas, Rafael AU - de Paola, Vincenzo AU - Barnes, Samuel J. AU - Sastre, Magdalena TI - Pharmacological ablation of astrocytes reduces A beta degradation and synaptic connectivity in an ex vivo model of Alzheimer's disease JF - JOURNAL OF NEUROINFLAMMATION J2 - J NEUROINFLAMM VL - 18 PY - 2021 IS - 1 PG - 12 SN - 1742-2094 DO - 10.1186/s12974-021-02117-y UR - https://m2.mtmt.hu/api/publication/32287941 ID - 32287941 AB - BackgroundAstrocytes provide a vital support to neurons in normal and pathological conditions. In Alzheimer's disease (AD) brains, reactive astrocytes have been found surrounding amyloid plaques, forming an astrocytic scar. However, their role and potential mechanisms whereby they affect neuroinflammation, amyloid pathology, and synaptic density in AD remain unclear.MethodsTo explore the role of astrocytes on A beta pathology and neuroinflammatory markers, we pharmacologically ablated them in organotypic brain culture slices (OBCSs) from 5XFAD mouse model of AD and wild-type (WT) littermates with the selective astrocytic toxin L-alpha-aminoadipate (L-AAA). To examine the effects on synaptic circuitry, we measured dendritic spine number and size in OBCSs from Thy-1-GFP transgenic mice incubated with synthetic A beta 42 or double transgenics Thy-1-GFP/5XFAD mice treated with LAAA or vehicle for 24 h.ResultsTreatment of OBCSs with L-AAA resulted in an increased expression of pro-inflammatory cytokine IL-6 in conditioned media of WTs and 5XFAD slices, associated with changes in microglia morphology but not in density. The profile of inflammatory markers following astrocytic loss was different in WT and transgenic cultures, showing reductions in inflammatory mediators produced in astrocytes only in WT sections. In addition, pharmacological ablation of astrocytes led to an increase in A beta levels in homogenates of OBCS from 5XFAD mice compared with vehicle controls, with reduced enzymatic degradation of A beta due to lower neprilysin and insulin-degrading enzyme (IDE) expression. Furthermore, OBSCs from wild-type mice treated with L-AAA and synthetic amyloid presented 56% higher levels of A beta in culture media compared to sections treated with A beta alone, concomitant with reduced expression of IDE in culture medium, suggesting that astrocytes contribute to A beta clearance and degradation. Quantification of hippocampal dendritic spines revealed a reduction in their density following L-AAA treatment in all groups analyzed. In addition, pharmacological ablation of astrocytes resulted in a decrease in spine size in 5XFAD OBCSs but not in OBCSs from WT treated with synthetic A beta compared to vehicle control.ConclusionsAstrocytes play a protective role in AD by aiding A beta clearance and supporting synaptic plasticity. LA - English DB - MTMT ER - TY - JOUR AU - Song, Zhenyan AU - Luo, Deyong AU - Wang, Yuke AU - Zheng, Yushan AU - Chen, Peiying AU - Xia, Xiaofang AU - He, Chunxiang AU - Yu, Wenjing AU - Li, Ping AU - Xiao, Chen AU - Cheng, Shaowu TI - Neuroprotective Effect of Danggui Shaoyao San via the Mitophagy-Apoptosis Pathway in a Rat Model of Alzheimer's Disease JF - EVIDENCE-BASED COMPLEMENTARY AND ALTERNATIVE MEDICINE J2 - EVID-BASED COMPL ALT VL - 2021 PY - 2021 PG - 11 SN - 1741-427X DO - 10.1155/2021/3995958 UR - https://m2.mtmt.hu/api/publication/33008068 ID - 33008068 AB - Alzheimer's disease (AD) is a serious neurodegenerative disease. While the main pathological characteristic of AD is widely believed to be the accumulation of amyloid-beta (A beta) in neurons around neurofibrillary plaques, the molecular mechanism of pathological changes is not clear. Traditional Chinese medicine offers many treatments for AD. Among these, Danggui Shaoyao San (DSS) is a classic prescription. In this study, an AD model was established by injecting A beta 1-42 into the brains of rats, which were then treated with different concentrations of Danggui Shaoyao San (sham operation; model; and Danggui Shaoyao San high-dose, medium-dose, and low-dose intervention groups). The Morris water maze test was used to assess the learning and memory abilities of the animals in each group. Nissl staining was used to detect neurons. Mitophagy was evaluated by transmission electron microscopy and immunofluorescence colocalization. Apoptosis was assessed by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. The expression levels of autophagy- and apoptosis-related proteins were measured by western blot. Compared to the model group, the groups of AD rats administered medium and high doses of Danggui Shaoyao San showed significantly increased learning and memory abilities (P<0.05), as well as significantly increased autophagosomes in the hippocampus. Moreover, the expression of PTEN-induced kinase 1 (PINK1), Parkin, and microtubule-associated protein light chain 3 (LC3-I/LC3-II) was increased, while that of p62 was significantly decreased (P<0.05). The neuronal apoptosis rate was also significantly decreased, the Bcl-2/Bax ratio was significantly increased, and the cleaved caspase-3 protein expression was significantly decreased (P<0.05). Therefore, Danggui Shaoyao San inhibited neuronal apoptosis in AD rats via a mechanism that may be related to the activation of the PINK1-Parkin-mediated mitophagy signaling pathway. LA - English DB - MTMT ER - TY - JOUR AU - Khonacha, Shima Ebrahimi AU - Janahmadi, Mahyar AU - Motamedi, Fereshteh TI - Kisspeptin-13 Improves Spatial Memory Consolidation and Retrieval against Amyloid-beta Pathology JF - IRANIAN JOURNAL OF PHARMACEUTICAL RESEARCH J2 - IRAN J PHARM RES VL - 18 PY - 2019 IS - Suppl. 1 SP - 169 EP - 181 PG - 13 SN - 1735-0328 DO - 10.22037/ijpr.2019.112199.13599 UR - https://m2.mtmt.hu/api/publication/31568811 ID - 31568811 AB - It has been shown that brain glucose metabolism impairment, obesity, and diabetes could lead to cognitive decline and Alzheimer's disease (AD) pathogenesis. Kisspeptin (KP) a G-protein coupled receptor neuropeptide, has been suggested as a link between energy balance and reproduction. Some studies have shown that the attenuation of KP signaling decreases metabolism and energy expenditure. KP mRNAs and receptors are detected in the hippocampus and cause the promotion of excitatory synaptic responses through modulation of postsynaptic signaling. The purpose of this study was to investigate the effect of KP on spatial learning and memory and its possible neuroprotective effect on Amyloid-Beta induced cognitive impairment using the Morris Water Maze (MWM) task in rats. The reference and reversal spatial learning and memory have been measured in this study. Rats were injected bilaterally by A01-42 (2 mu g/mu L) or saline as a vehicle into the hippocampal CA1 area. One week later, KP-13 (1.5 or 2 mu g/mu L) was injected i.c.v before or after each training session for 3 days and memory was tested 24 h later. The results showed KP-13 by itself could significantly enhance spatial memory consolidation and retrieval, and A beta induced reversal and reference memory impairment was significantly ameliorated by KP-13. In Conclusion, it seems that KP-13 as a neuropeptide has to enhance spatial memory properties and could be a possible neuroprotective peptide on amyloid-beta induced pathology. LA - English DB - MTMT ER - TY - JOUR AU - Szögi, Titanilla AU - Schuster, Ildikó AU - Borbély, Emőke AU - Gyebrovszki, Andrea AU - Bozsó, Zsolt AU - Gera, Janos AU - Rajkó, Róbert AU - Sántha, Miklós AU - Penke, Botond AU - Fülöp, Lívia TI - Effects of the Pentapeptide P33 on Memory and Synaptic Plasticity in APP/PS1 Transgenic Mice: A Novel Mechanism Presenting the Protein Fe65 as a Target JF - INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES J2 - INT J MOL SCI VL - 20 PY - 2019 IS - 12 PG - 20 SN - 1661-6596 DO - 10.3390/ijms20123050 UR - https://m2.mtmt.hu/api/publication/30744451 ID - 30744451 AB - Regulated intramembrane proteolysis (RIP) of the amyloid precursor protein (APP) leads to the formation of fragments, among which the intracellular domain of APP (AICD) was also identified to be a causative of early pathological events. AICD-counteracting proteins, such as Fe65, may serve as alternative therapeutic targets of Alzheimer's disease (AD). The detection of elevated levels of Fe65 in the brains of both human patients and APP transgenic mice may further strengthen the hypothesis that influencing the interaction between Fe65 and APP may have a beneficial effect on the course of AD. Based on a PXP motif, proven to bind to the WW domain of Fe65, a new pentapeptide was designed and tested. The impedimental effect of P33 on the production of beta amyloid (A beta) (soluble fraction and aggregated plaques) and on the typical features of the AD pathology (decreased dendritic spine density, synaptic markers, elevated inflammatory reactions) was also demonstrated. Significant enhancements of both learning ability and memory function were observed in a Morris water maze paradigm. The results led us to formulate the theory that P33 acts by altering the conformation of Fe65 via binding to its WW domain, consequently hindering any interactions between Fe65 and key members involved in APP processing. LA - English DB - MTMT ER - TY - JOUR AU - Gupta, Smriti AU - Yadav, Kamalendra AU - Mantri, Shrikant S. AU - Singhal, Nitin K. AU - Ganesh, Subramaniam AU - Sandhir, Rajat TI - Evidence for Compromised Insulin Signaling and Neuronal Vulnerability in Experimental Model of Sporadic Alzheimer's Disease JF - MOLECULAR NEUROBIOLOGY J2 - MOL NEUROBIOL VL - 55 PY - 2018 IS - 12 SP - 8916 EP - 8935 PG - 20 SN - 0893-7648 DO - 10.1007/s12035-018-0985-0 UR - https://m2.mtmt.hu/api/publication/30542819 ID - 30542819 AB - Evidence from animal studies categorizes sporadic Alzheimer's disease (sAD) as a metabolic syndrome with accompanying cognitive deficits. Given that glial cells act as silent partners to neurons by providing trophic support and defense, the present study investigated the role of glia in sAD pathology. A streptozotocin (STZ)-induced glial-neuronal co-culture model of sAD was used to study the metabolic status of the two cell types. Real timeRT-PCR and Western blotting results indicated that amyloid precursor protein (APP) and -secretase (BACE1) were highly expressed in co-cultured neurons than in monocultures. Increased amyloidogenesis was accompanied by decreased expression of mediators in insulin signaling pathway that included insulin receptor (IR), insulin receptor substrate2 (IRS2), insulin-like growth factor2 (IGF2), insulin-like growth factor1 receptor (IGF1R), total-glycogen synthase kinase 3 (t-GSK3), and phosphorylated-GSK3(ser9) (p-GSK3(ser9)), suggesting that neuronal cells are more prone to metabolic variability when cultured in the presence of glial cells. Findings from the sAD model induced by intracerebroventricular (ICV) injection of STZ revealed that increased amyloid beta (A) load in the hippocampus was potentially responsible for the hyperphosphorylation of tau at ser(396). Furthermore, impaired cognitive functions and decreased dendritic spine density and axonal thinningin CA1region of hippocampus wereassociated with decreased IR and p-GSK3(ser9)/t-GSK3 expression. Taken together, the presentstudy provides evidence that glia mediated responseand insulinsignaling defects drive pathological changes in sAD and represent potentialtargets for delaying sAD progression. LA - English DB - MTMT ER - TY - JOUR AU - Han, Fei AU - Zhuang, Ting-Ting AU - Chen, Jing-Jing AU - Zhu, Xiu-Ling AU - Cai, Ya-Fei AU - Lu, Ya-Ping TI - Novel derivative of Paeonol, Paeononlsilatie sodium, alleviates behavioral damage and hippocampal dendritic injury in Alzheimer's disease concurrent with cofilin1/phosphorylated-cofilin1 and RAC1/CDC42 alterations in rats JF - PLOS ONE J2 - PLOS ONE VL - 12 PY - 2017 IS - 9 PG - 24 SN - 1932-6203 DO - 10.1371/journal.pone.0185102 UR - https://m2.mtmt.hu/api/publication/26918263 ID - 26918263 LA - English DB - MTMT ER - TY - JOUR AU - Kasza, Ágnes AU - Penke, Botond AU - Frank, Z AU - Bozsó, Zsolt AU - Szegedi, Viktor AU - Hunya, Ákos AU - Nemeth, K AU - Kozma, Gábor AU - Fülöp, Lívia TI - Studies for improving a rat model of Alzheimer's disease: ICV administration of well-characterized β-amyloid 1-42 oligomers induce dysfunction in spatial memory JF - MOLECULES J2 - MOLECULES VL - 22 PY - 2017 IS - 11 PG - 28 SN - 1420-3049 DO - 10.3390/molecules22112007 UR - https://m2.mtmt.hu/api/publication/3310819 ID - 3310819 N1 - N1 Funding details: GINOP-2.3.2-15-2016-00060 N1 Funding text: Acknowledgments: We are very grateful for László Siklós for the measurements of dendritic spine density. The authors express their thanks to Anita Kurunczi and Eszter Sipos for the studies on AMCA labeled Aβ fibrils. This work was supported by the EC Health Program “Memoload” (FP-7 project n◦ 201.159) and the Hungarian NKFIH research grant GINOP-2.3.2-15-2016-00060. LA - English DB - MTMT ER - TY - CHAP AU - Mishra, Neha AU - Singh, Rameshwar AU - Sharma, Deepak ED - Pramod, C. Rath ED - Ramesh, Sharma ED - Prasad, S TI - Changes in Social Behavior Associated with Alzheimer’s Disease-Related Aβ Pathology T2 - Topics in Biomedical Gerontology PB - Springer-Verlag Singapore CY - Singapore SN - 9789811021558 PY - 2017 SP - 253 EP - 265 PG - 13 DO - 10.1007/978-981-10-2155-8_13 UR - https://m2.mtmt.hu/api/publication/34549695 ID - 34549695 LA - English DB - MTMT ER - TY - JOUR AU - Zhao, Fengyan AU - Qu, Yi AU - Zhu, Jianghu AU - Zhang, Li AU - Huang, Lan AU - Liu, Haiting AU - Li, Shiping AU - Mu, Dezhi TI - miR-30d-5p Plays an Important Role in Autophagy and Apoptosis in Developing Rat Brains After Hypoxic-Ischemic Injury JF - JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY J2 - J NEUROPATH EXP NEUR VL - 76 PY - 2017 IS - 8 SP - 709 EP - 719 PG - 11 SN - 0022-3069 DO - 10.1093/jnen/nlx052 UR - https://m2.mtmt.hu/api/publication/26918264 ID - 26918264 LA - English DB - MTMT ER - TY - JOUR AU - Jin, Huafeng AU - Chen, Tingting AU - Li, Guoxi AU - Wang, Conghui AU - Zhang, Baofeng AU - Cao, Xinyuan AU - Sha, Sha AU - Wan, Qi AU - Chen, Ling TI - Dose-Dependent Neuroprotection and Neurotoxicity of Simvastatin through Reduction of Farnesyl Pyrophosphate in Mice Treated with Intracerebroventricular Injection of A beta(1-42) JF - JOURNAL OF ALZHEIMER'S DISEASE J2 - J ALZHEIMERS DIS VL - 50 PY - 2016 IS - 2 SP - 501 EP - 516 PG - 16 SN - 1387-2877 DO - 10.3233/JAD-150782 UR - https://m2.mtmt.hu/api/publication/25428934 ID - 25428934 LA - English DB - MTMT ER - TY - JOUR AU - Park, Sunmin AU - Kang, Suna AU - Kim, Da Sol AU - Moon, Bo Rerum TI - Agrimonia pilosa Ledeb., Cinnamomum cassia Blume, and Lonicera japonica Thunb . protect against cognitive dysfunction and energy and glucose dysregulation by reducing neuroinflammation and hippocampal insulin resistance in β -amyloid-infused rats JF - NUTRITIONAL NEUROSCIENCE J2 - NUTR NEUROSCI VL - 20 PY - 2016 IS - 2 SP - 77 EP - 88 PG - 12 SN - 1028-415X DO - 10.1080/1028415X.2015.1135572 UR - https://m2.mtmt.hu/api/publication/34549593 ID - 34549593 LA - English DB - MTMT ER - TY - JOUR AU - Yi, Mengni AU - Yu, Panpan AU - Lu, Qin AU - Geller, Herbert M AU - Yu, Zhihua AU - Chen, Hongzhuan TI - KCa3.1 constitutes a pharmacological target for astrogliosis associated with Alzheimer's disease JF - MOLECULAR AND CELLULAR NEUROSCIENCE J2 - MOL CELL NEUROSCI VL - 76 PY - 2016 SP - 21 EP - 32 PG - 12 SN - 1044-7431 DO - 10.1016/j.mcn.2016.08.008 UR - https://m2.mtmt.hu/api/publication/26224479 ID - 26224479 LA - English DB - MTMT ER - TY - JOUR AU - Arsalandeh, Farshad AU - Ahmadian, Shahin AU - Foolad, Forough AU - Khodagholi, Fariba AU - Farimani, Mahdi M AU - Shaerzadeh, Fatemeh TI - Beneficial Effect of Flavone Derivatives on A-Induced Memory Deficit Is Mediated by Peroxisome Proliferator-Activated Receptor Coactivator 1: A Comparative Study JF - INTERNATIONAL JOURNAL OF TOXICOLOGY J2 - INT J TOXICOL VL - 34 PY - 2015 IS - 3 SP - 274 EP - 283 PG - 10 SN - 1091-5818 DO - 10.1177/1091581815584165 UR - https://m2.mtmt.hu/api/publication/24889307 ID - 24889307 LA - English DB - MTMT ER - TY - JOUR AU - Salgado-Puga, K AU - Pena-Ortega, F TI - Cellular and Network Mechanisms Underlying Memory Impairment Induced by Amyloid beta Protein JF - PROTEIN AND PEPTIDE LETTERS J2 - PROTEIN PEPTIDE LETT VL - 22 PY - 2015 IS - 4 SP - 303 EP - 321 PG - 19 SN - 0929-8665 DO - 10.2174/0929866522666150202112154 UR - https://m2.mtmt.hu/api/publication/27196666 ID - 27196666 LA - English DB - MTMT ER - TY - JOUR AU - Tong, Jia-qing AU - Zhang, Jun AU - Hao, Ming AU - Yang, Ju AU - Han, Yu-fei AU - Liu, Xiao-jie AU - Shi, Hui AU - Wu, Mei-na AU - Liu, Qing-song AU - Qi, Jin-shun TI - Leptin attenuates the detrimental effects of beta-amyloid on spatial memory and hippocampal later-phase long term potentiation in rats JF - HORMONES AND BEHAVIOR J2 - HORM BEHAV VL - 73 PY - 2015 SP - 125 EP - 130 PG - 6 SN - 0018-506X DO - 10.1016/j.yhbeh.2015.06.013 UR - https://m2.mtmt.hu/api/publication/25428505 ID - 25428505 LA - English DB - MTMT ER -