En la predela surge un relieve x mm de Santa Teresa dentro de una mandorla rectangular, todo ello elaborado de una forma muy sencilla. En la mano izquierda lleva un libro y en la derecha le faltan las llaves". Se encuentra enmarcado en una especie de mandorla rematada por un grutesco de motivos vegetales".
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La iglesia parroquial de la villa cuenta con dos pergaminos realizados durante la Edad Media y relativos a la vida monacal:. Ello es debido al corte o tijeretazo que ha sufrido el pergamino. El segundo pergamino fue empleado como forro para un grueso tomo de documentos con sello real en tinta que data del siglo XVIII y se conserva en el Archivo Diocesano de Astorga. La casa solariega , edificio principal de planta cuadrada, tiene su entrada en su cara este. Destaca, asimismo, la balconada y corredor que se abren en la cara oeste de la casa y dan a la gran finca que compone el complejo.
En la segunda planta se hallaban las habitaciones y se pueden ver los vestigios de una capilla. Casi todos los festejos del pueblo se llevan a cabo dentro de esta imponente finca. De planta cuadrada, dispone de tres alturas y un bajo cubierta. De propiedad privada, situada en la confluencia de la calle Mayor con la plaza central del pueblo.
Estos aprovechaban la fuerza de la abundante agua para mover sus ruedas de molienda.
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Ambos asentados sobre la acequia que cruza el pueblo en sentido este-oeste. Se encontraba en la entrada del pueblo, en la que, actualemente, es la plaza de la Ermita. Hoy desaparecida, como recuerdo de la misma, en el presente solo encontramos una cruz sobre un pedestal en dicha plazuela. Esta ermita contaba con una imagen de San Antonio, de la cual se desconoce su destino.
Se encontraba junto a la ermita de San Antonio y a escasos metros del Camino Real junto a la hermita Tenemos otra noticia documental sobre este paraje: D. La rica vega del Boeza compensa lo desfavorable del clima permitiendo una gran abundancia de pastos para el ganado y cultivos muy diversos.
Todo ello dota a la villa de un ritmo que en otras muchas localidades se ha perdido hace largo tiempo. Casi exclusivamente representado por los bares de la localidad y una tienda de ultramarinos.
En tiempos pasados era, incluso, muy frecuente encontrar peces en las acequias y canales de riego que recorren el territorio de la villa. Consultado el 28 de agosto de De Wikipedia, la enciclopedia libre. Albares de la Ribera. Digo yo Dn. Miguel de Olano firmado y rubricado. Sub Christi nomine completus fuit iste liber sub umbra- culo Sancte Marie et Sancti Martini in monas- terio vocabulo Alba- res. Felix ille Obsecro vos, qui legeritis, mei, Johannis peccatoris memineritis, quatenus per misericordiam domino nostri Jesu Christi et vestris orationibus merear a propriis expiari facinoribus atque in libro vite cum electis adnotari confessoribus, amen.
Joannes, diaconus, fecit et pinxit. Qui legerit, oret pro peccatore, si Christo habeat protectore et in omnibus adjutore. O lector, dum legis ora pro scriptore, si Christum habeas protectore, cuando dominus noster rogaveritis. Joannis diaconus fecit. Factum series testamenti undecimo kalendas decembris, era octogessima secunda super millessima.
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Unfortunately, the drugs available for the treatment of dementia are not cost-effective. Future anti-dementia drugs must address the complex pathogenic niche of the disease from a multifactorial perspective. In addition to anti-dementia drugs, patients with AD, or with other forms of dementia, need concomitant medications for the treatment of diverse disorders of the central nervous system CNS associated with progressive brain dysfunction.
Although many genes have been suggested to be associated with AD, with the exception of APOE, most polymorphic variants of potential risk exhibit a very weak association with AD. Drug metabolism, and the mechanisms underlying drug efficacy and safety, are also genetically regulated complex traits in which hundreds of genes cooperatively participate. There are over different types of dementia with a common phenotypic denominator composed of cognitive and mental deterioration, psychomotor dysfunction, behavioural changes, and progressive functional decline 1.
AD is a complex disorder in which multiple pathogenic mechanisms may be involved giving rise to a common phenotype. From a didactic point of view, it has been established that primary pathogenic events in AD are represented by genetic factors mutations, susceptibility SNPs and programmed neuronal death, since neurons start to die years before the onset of the disease. Secondary pathogenic events are associated with the phenotypic expression of senile plaques amyloid deposition and neur of ibrillary tangles NFT , together with synaptic loss, dendritic desarborization, and neuronal death, as the major hallmarks of AD pathology.
Tertiary and quaternary pathogenic events are reflected by neurotransmitter deficits, neuroinflammatory reactions, oxidative stress phenomena and free radical formation, excitotoxic reactions, alterations in calcium homeostasis, deficit of neurotrophic factors, and cerebrovascular perturbations, among many other neurochemical phenotypes All these pathogenic elements configure the AD phenotype which differs from that of the healthy elderly population.
The phenotypic features of the disease represent the biomarkers to be modified with an effective therapeutic intervention Fig. Blood pressure values, glucose levels and cholesterol levels are higher in AD than in healthy elderly subjects Table 1.
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Significant differences are currently seen between females and males, indicating the effect of gender on the phenotypic expression of the disease. All these parameters are highly relevant when treating AD patients because some of them reflect a concomitant pathology which also needs therapeutic consideration. On the other hand, they can also represent general biomarkers together with regional brain atrophy and perfusion and cognitive function, which may serve as therapeutic outcome measures. Notwithstanding, the complexity of the pathogenic cascade in AD invites the prediction that many other genetic factors and pathogenic mechanisms may be involved in the etiology of AD, together with epigenetic phenomena, cerebrovascular dysfunction, and environmental events 12 Fig.
There are roughly million positions in the human genome that can show variability among individuals, and differences in the DNA sequence are the genetic basis of human variability and complex traits. Segmental duplications frequently mediate polymorphic rearrangements of intervening sequences via non-allelic homologous recombination NAHR with major implications for human disease. The differential expression of common variants is a major source of genetic variation with important repercussions in human diversity and disease heterogeneity.
Prior to the completion of the Human Gen ome Project and the emergence of dense genetic maps, scientists used linkage studies and positional cloning to identify DNA mutations in rare diseases, but in the past two decades association study designs became more powerful compared with linkage Fig. Currently, over 10 million DNA sequence variations have been uncovered in the human genome It has been observed that the genetic variation rate GVR is higher in AD patients than in the general population 12,14, Increased GVR in AD might indicate that the over-representation of a series of genes involved in brain maturation and in the maintenance of higher activities of the CNS has surpassed a natural selection threshold excessive genome complexity, genomic overdiversification , constituting a Darwinian disadvantage which shortens life span in humans 12, Recent studies with alignments of 10, human genes have identified protein-coding sequences with an accelerated rate of base substitutions along the human lineage.
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