La provisión de plazas en las escuelas públicas de primera enseñanza: fuentes documentales en el Archivo General de la Universidad Complutense de Madrid

El sistema educativo basado en la enseñanza elemental de carácter universal, gratuito y aplicable a todos los españoles con el objeto de fomentar su condición de ciudadanos, tiene su punto de partida en la Constitución de Cádiz. Posteriormente, la Ley de 1857 trazará los ejes que, durante más de un siglo, articularán la educación en España. Es, precisamente, la denominada Ley Moyano la que otorga a la Universidad y, por ende, al rector la competencia sobre la dotación de plazas vacantes en las escuelas públicas del distrito universitario de Madrid, que comprendía las provincias de Madrid, Ávila, Guadalajara, Toledo, Cuenca, Ciudad Real y Segovia, tanto por el sistema de concurso como por el de oposición. El procedimiento administrativo de provisión de plazas generó un importante volumen documental que se conserva en el Archivo General de la Universidad Complutense de Madrid. Ambos aspectos -procedimiento administrativo y documentos- constituyen el objeto de esta comunicación. Para finalizar, y como conclusión, se ha llevado a cabo un estudio pormenorizado de la documentación generada con motivo de los concursos y oposiciones que tuvieron lugar en el periodo 1880-1920, en las escuelas públicas de la provincia de Guadalajara

Historia del Archivo de la Universidad Complutense de Madrid (1836-2006)

UCM. Archivo General y Protección de DatosEdiciones ComplutenseTRUEpu

Olfactory bulb neuroproteomics reveals a chronological perturbation of survival routes and a disruption of prohibitin complex during Alzheimer’s disease progression

Olfactory dysfunction is among the earliest features of Alzheimer's disease (AD). Although neuropathological abnormalities have been detected in the olfactory bulb (OB), little is known about its dynamic biology. Here, OB-proteome analysis showed a stage-dependent synaptic proteostasis impairment during AD evolution. In addition to progressive modulation of tau and amyloid precursor protein (APP) interactomes, network-driven proteomics revealed an early disruption of upstream and downstream p38 MAPK pathway and a subsequent impairment of Phosphoinositide-dependent protein kinase 1 (PDK1)/Protein kinase C (PKC) signaling axis in the OB from AD subjects. Moreover, a mitochondrial imbalance was evidenced by a depletion of Prohibitin-2 (Phb2) levels and a specific decrease in the phosphorylated isoforms of Phb1 in intermediate and advanced AD stages. Interestingly, olfactory Phb subunits were also deregulated across different types of dementia. Phb2 showed a specific up-regulation in mixed dementia, while Phb1 isoforms were down-regulated in frontotemporal lobar degeneration (FTLD). However, no differences were observed in the olfactory expression of Phb subunits in progressive supranuclear palsy (PSP). To sum up, our data reflect, in part, the missing links in the biochemical understanding of olfactory dysfunction in AD, unveiling Phb complex as a differential driver of neurodegeneration at olfactory level

Early-Onset Molecular Derangements in the Olfactory Bulb of Tg2576 Mice: Novel Insights Into the Stress-Responsive Olfactory Kinase Dynamics in Alzheimer’s Disease

The olfactory bulb (OB) is the first processing station in the olfactory pathway. Despite smell impairment, which is considered an early event in Alzheimer's disease (AD), little is known about the initial molecular disturbances that accompany the AD development at olfactory level. We have interrogated the time-dependent OB molecular landscape in Tg2576 AD mice prior to the appearance of neuropathological amyloid plaques (2-, and 6-month-old), using combinatorial omics analysis. The metabolic modulation induced by overproduction of human mutated amyloid precursor protein (APP) clearly differs between both time points. Besides the progressive perturbation of the APP interactome, functional network analysis unveiled an inverse regulation of downstream extracellular signal-regulated kinase (ERK1/2), and p38 mitogen-activated protein kinase (MAPK) routes in 2-month-old Tg2576 mice with respect to wild-type (WT) mice. In contrast, Akt and MAPK kinase 4 (SEK1)/ stress-activated protein kinase (SAPK) axis were parallel activated in the OB of 6-months-old-Tg2576 mice. Furthermore, a survival kinome profiling performed during the aging process (2-, 6-, and 18-month-old) revealed that olfactory APP overexpression leads to changes in the activation dynamics of protein kinase A (PKA), and SEK1/MKK4-SAPK/JNK between 6 and 18 months of age, when memory deficits appear and AD pathology is well established in transgenic mice. Interestingly, both olfactory pathways were differentially activated in a stage-dependent manner in human sporadic AD subjects with different neuropathological grading. Taken together, our data reflect the early impact of mutated APP on the OB molecular homeostasis, highlighting the progressive modulation of specific signaling pathways during the olfactory amyloidogenic pathology

Amyloid-driven tau accumulation on mitochondria potentially leads to cognitive deterioration in alzheimer’s disease

Despite the well-accepted role of the two main neuropathological markers (β-amyloid and tau) in the progression of Alzheimer’s disease, the interaction and specific contribution of each of them is not fully elucidated. To address this question, in the present study, an adeno-associated virus (AAV9) carrying the mutant P301L form of human tau, was injected into the dorsal hippocampi of APP/PS1 transgenic mice or wild type mice (WT). Three months after injections, memory tasks, biochemical and immunohistochemical analysis were performed. We found that the overexpression of hTauP301L accelerates memory deficits in APP/PS1 mice, but it did not affect memory function of WT mice. Likewise, biochemical assays showed that only in the case of APP/PS1-hTauP301L injected mice, an important accumulation of tau was observed in the insoluble urea fraction. Similarly, electron microscopy images revealed that numerous clusters of tau immunoparticles appear at the dendrites of APP/PS1 injected mice and not in WT animals, suggesting that the presence of amyloid is necessary to induce tau aggregation. Interestingly, these tau immunoparticles accumulate in dendritic mitochondria in the APP/PS1 mice, whereas most of mitochondria in WT injected mice remain free of tau immunoparticles. Taken together, it seems that amyloid induces tau aggregation and accumulation in the dendritic mitochondria and subsequently may alter synapse function, thus, contributing to accelerate cognitive decline in APP/PS1 mice.We gratefully acknowledge grant funding support from Ministry of Science and Innovation (MINECO) with exp. PID2019-104921RB-I00/MCI/AEI/10.13039/501100011033 as well as to the Foundation for Applied Medical Research, the University of Navarra (Pamplona, Spain) for financial support and the Asociación de Amigos of the University of Navarra for the grant to M.P.-G. and S.B. We also gratefully acknowledge grant funding support from Spanish Ministerio de Economía y Competitividad (RTI2018-095812-B-I00 MCIN/ AEI/10.13039/501100011033) y por FEDER una manera de hacer Europa and Junta de Comunidades de Castilla-La Mancha (SBPLY/17/180501/000229) to RL, from the Spanish Ministry of Science Innovation and Universities (Ref. PID2019-110356RB-I00/AEI/10.13039/501100011033) to J.F.-I. and E.S and from the Department of Economic and Business Development from Government of Navarra (INNOLFACT project; Ref. 0011-1411-2020-000028)

Transetosomas como sistema de encapsulación de Agastache mexicana

El uso de plantas como Agastache mexicana en el tratamiento fitoterapéutico ante diferentes afecciones como trastornos relacionados al sistema nervioso central, enfermedades gastrointestinales y cardiovasculares, ha dado origen a la búsqueda de sistemas de encapsulación que aseguren el atrapamiento, la liberación, la manejabilidad y preservación de sus compuestos activos. En este trabajo se propone a los transetosomas como matriz de encapsulación debido a su biocompatibilidad, capacidad de atrapamiento entre otras propiedades fisicoquímicas atribuidas a su tamaño submicrométrico. Se logró encapsular un extracto etanólico de Agastache mexicana en transetosomas con un tamaño de 722nm, y morfología esférica, se caracterizó mediante microscopía electrónica de barrido y microscopía DIC, mediante microscopía de fluorescencia y espectrometría FT-IR se comprobó el atrapamiento del extracto. Se comprobó que los transetosomas son capaces de encapsular un extracto etanólico de A. mexicana, con lo que se pretende que estos sistemas puedan ser utilizados en extractos de plantas semejantes.The use of Agastache mexicana as a phytotherapeutic treatment for different affections such as disorders of the central nervous system, gastrointestinal and cardiovascular diseases has led to the search for encapsulation systems that ensure the entrapment, release, manipulation and preservation of the active compounds. In this work, there are proposed the transethosomes as encapsulation matrix, due to its biocompatibility, entrapment capacity among other physicochemical properties attributed to its submicrometric size. It was possible to encapsulate an ethanolic extract of Agastache mexicana, in transethosomes with a size of 722nm and spherical morphology, was characterized by scanning electron microscopy, DIC microscopy and by fluorescence microscopy and FT-IR spectrometry. It was verified that the transethosomes can encapsulate an ethanolic extract of A. mexicana, with what it is intended that these systems be used in similar plant extracts