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Promotion of structural plasticity in area V2 of visual cortex prevents against object recognition memory deficits in aging and Alzheimer's disease rodents

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Neural Regeneration Research 2024年第8期19卷 1835-1841页

作者： Irene Navarro-Lobato Mariam Masmudi-Martín Manuel F.López-Aranda Juan F.López-Téllez Gloria Delgado Pablo Granados-Durán Celia Gaona-Romero Marta Carretero-Rey Sinforiano Posadas María E.Quiros-Ortega Zafar U.Khan Laboratory of Neurobiology Centro de Investigaciones Médico Sanitarias(CIMES)University of MalagaMalagaSpain Department of Medicine Faculty of MedicineUniversity of MalagaMalagaSpain Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas(CIBERNED) Institute of Health Carlos IIIMadridSpain the Donders Institute for Brain Cognition and Behaviour Radboud UniversityNijmegenThe Netherlands the Brain Metastasis Group National Cancer Research Centre(CNIO)MadridSpain the Department of Neurobiology University of California-Los AngelesLos AngelesCAUSA

Memory deficit,which is often associated with aging and many psychiatric,neurological,and neurodegenerative diseases,has been a challenging issue for *** till now,all potential drug candidates have failed to produce satisfa ctory ***,in the search for a solution,we found that a treatment with the gene corresponding to the RGS14414protein in visual area V2,a brain area connected with brain circuits of the ventral stream and the medial temporal lobe,which is crucial for object recognition memory(ORM),can induce enhancement of *** this study,we demonstrated that the same treatment with RGS14414in visual area V2,which is relatively unaffected in neurodegenerative diseases such as Alzheimer s disease,produced longlasting enhancement of ORM in young animals and prevent ORM deficits in rodent models of aging and Alzheimer’s ***,we found that the prevention of memory deficits was mediated through the upregulation of neuronal arbo rization and spine density,as well as an increase in brain-derived neurotrophic factor(BDNF).A knockdown of BDNF gene in RGS14414-treated aging rats and Alzheimer s disease model mice caused complete loss in the upregulation of neuronal structural plasticity and in the prevention of ORM *** findings suggest that BDNF-mediated neuronal structural plasticity in area V2 is crucial in the prevention of memory deficits in RGS14414-treated rodent models of aging and Alzheimer’s ***,our findings of RGS14414gene-mediated activation of neuronal circuits in visual area V2 have therapeutic relevance in the treatment of memory deficits.

关键词： behavioral performance brain-derived neurotrophic factor cognitive dysfunction episodic memory memory circuit activation memory deficits memory enhancement object recognition memory prevention of memory loss regulator of G protein signaling

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Implication of 14-3-3ζ-BDNF pathway in long-lasting memory enhancement and the rescue from memory deficits

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Neural Regeneration Research 2022年第12期17卷 2685-2686页

作者： Mariam Masmudi-Martín Irene Navarro-Lobato Zafar U.Khan Brain Metastasis Group National Cancer Research Centre(CNIO)MadridSpain Donders Institute for Brain Cognition and Behaviour Radboud UniversityNijmegenThe Netherlands Laboratory of Neurobiology CIMESUniversity of MalagaMalagaSpain Department of Medicine Faculty of MedicineUniversity of MalagaMalagaSpain CIBERNED Institute of Health Carlos ⅢMadridSpain

Intact memory function is critical for carrying out daily life activities,such as managing finances,remembering to take medications,driving in familiar environments,remembering a grandchild’s birthday,and learning to use a new ***,memory deficits not only accompany normal aging but are also comorbid with many psychiatric,neurological,and neurodegenerative *** disability,autism,attention deficit disorder,learning disability,schizophrenia,and depression all have memory deficit components,as do Alzheimer’s disease,Parkinson’s disease,Huntington’s disease,and other neurodegenerative diseases(Khan et al.,2014).Therefore,a large proportion of the human population is affected by this brain disorder.

关键词： Huntington remember finance

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Triglyceride levels and apolipoprotein E polymorphism in patients with acute pancreatitis

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Hepatobiliary & Pancreatic Diseases International 2012年第1期11卷 96-101页

作者： Radka Ivanova Susana Puerta Alfonso Garrido Ignacio Cueto Ana Ferro María José Ariza Andrés Cobos Pedro González-Santos Pedro Valdivielso Division of Internal Medicine Hospital Universitario "Virgen de la Victoria" Division of Gastroenterology Hospital Universitario "Virgen de la Victoria" cimes Department of Medicine & Dermatology University of Malaga Division of Laboratory Hospital Universitario "Virgen de la Victoria"

BACKGROUND:Hypertriglyceridemia is an unusual cause of acute pancreatitis and sometimes considered to be an *** study aimed to investigate the clinical and analytical features and the APOE genotypes in patients with acute pancreatitis and severe ***:We undertook a one-year,prospective study of patients with acute pancreatitis whose first laboratory analysis on admission to the emergency department included measurement of serum *** APOE genotype was determined and the patients answered an established questionnaire within the first 24 hours concerning their alcohol consumption,the presence of co-morbidities and any medications being *** patients’ progression,etiological diagnosis,hospital stay and clinical and radiological severity were all ***:Hypertriglyceridemia was responsible for 7 of 133 cases of pancreatitis (5%);the remaining cases were of biliary (53%),idiopathic (26%),alcoholic (11%) or other (5%) *** with these remaining cases,the patients with hypertriglyceridemia were significantly younger,had more relapses,and more often had diabetes *** usually consumed alcohol or consumed it excessively on the days before ***,the ε4 allele of the APOE gene was more common in this group (P<0.05).CONCLUSION:One of 20 episodes of acute pancreatitis is caused by hypertriglyceridemia and it is linked to genetic (ε4 allele) and comorbid factors such as diabetes and,especially,alcohol consumption.

关键词： acute pancreatitis hypertriglyceridemia apolipoprotein E alcohol biliary lithiasis

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