Transexualidad y reproducción: situación actual desde el punto de vista clínico y legal / Transsexualism and reproduction: Clinical and legal situation

Se diagnostican como transexuales las personas que se identifican con el sexo opuesto y rechazan el género propio. Existen distintas hipótesis que intentan explicar el origen de la transexualidad, siendo las más aceptadas las teorías con bases biológicas. La prevalencia estimada es variable en función de la zona geográfica, siendo más frecuentes los transexuales femeninos que los masculinos. Las técnicas de reproducción asistida facilitan las opciones reproductivas de este colectivo que acude, cada vez más, a los centros clínicos especializados para tratar de formar una familia defendiendo el derecho a la reproducción de todo ser humano. Los transexuales pueden verse favorecidos especialmente por las técnicas de preservación de la fertilidad, pudiendo criopreservar sus gametos antes de la reasignación de sexo como estrategia preventiva en vistas a un posible deseo de reproducción futura. La falta de recomendaciones o guías consensuadas sobre la aplicabilidad de las técnicas de reproducción asistida en individuos transexuales y el vacío normativo existente dificultan su acceso a estas técnicas. Esta revisión recoge las posibles opciones reproductivas de los transexuales desde un punto de vista clínico y analiza la situación actual en el marco de la legislación española vigente (AU)

People who identify themselves with the opposite sex and reject their own gender are diagnosed as transsexuals. Different hypotheses have tried to explain the origin of transsexualism, biological theories being the most accepted. The estimated prevalence is variable, this depending on the geographic area. Female are more frequent than male transsexuals. Assisted reproduction techniques facilitate the reproductive options of this group who increasingly come to specialized clinical centers to try to form a family, defending the reproductive rights of every human being. Transsexuals could be especially favored by fertility preservation techniques, being able to cryopreserve their gametes before sex reassignment as a preventive strategy in view of a possible desire for future reproduction. Lack of recommendations or agreed on guidelines and absence of regulations about the applicability of assisted reproduction in transsexuals hinders their access to these techniques. This review summarizes the possible reproductive options of transsexuals from a clinical point of view and analyzes the current situation in the framework of Spanish law (AU)

Triheptanoin supplementation to ketogenic diet curbs cognitive impairment in APP/PS1 mice used as a model of familial Alzheimer's disease.

Diets containing a high proportion of fat with respect to protein plus carbohydrates are capable of inducing ketone body production in the liver, which provides an energetic alternative to glucose. Some ketogenic diets have been tested as therapeutic strategies for treating metabolic disorders related to a deficiency in glucose-driven ATP generation. However, ketone bodies are not capable of providing extra tricarboxylic acid cycle intermediates, limiting the anabolic capacity of the cell. Therefore, it is reasonable to hypothesize that supplementing a ketogenic diet with anaplerotic compounds such as triheptanoin may improve ketogenic diet effectiveness. The present study tests this hypothesis in APP/PS1 (APPswe/PS1dE9) transgenic mice, used as a model of familial Alzheimer's disease because impaired energy supply to neurons has been linked to this neurodegenerative process. Triheptanoin supplementation to a ketogenic diet for three months and starting at the age of three months reduces the memory impairment of APP/PS1 mice at the age of 6 months. The Aß production and deposition were not significantly altered by the ketogenic diet, supplemented or not by triheptanoin. However, mice fed with triheptanoin-rich ketogenic diet have shown decreased astroglial response in the vicinity of Aß plaques and decreased expression of the pro-inflammatory cytokine interferon-γ in astrocytes. These findings correlate with transcriptional up-regulation of the ROS detoxifying mechanisms Sirt1 and Pparg, thus linking triheptanoin with improved mitochondrial status. Present findings support the concept that ketogenic diets supplemented with anaplerotic compounds can be considered potential therapeutic strategies at early stages of Alzheimer's disease.

Amyloid generation and dysfunctional immunoproteasome activation with disease progression in animal model of familial Alzheimer's disease.

Double-transgenic amyloid precursor protein/presenilin 1 (APP/PS1) mice express a chimeric mouse/human APP bearing the Swedish mutation (Mo/HuAPP695swe) and a mutant human PS1-dE9 both causative of familial Alzheimer's disease (FAD). Transgenic mice show impaired memory and learning performance from the age of 6 months onwards. Double-transgenic APP/PS1 mice express altered APP and PS1 mRNAs and proteins, reduced ß-secretase 1 (BACE1) mRNA and normal BACE1 protein, all of which suggest a particular mechanism of amyloidogenesis when compared with sporadic AD. The first ß-amyloid plaques in APP/PS1 mice appear at 3 months, and they increase in number and distribution with disease progression in parallel with increased levels of brain soluble ß-amyloid 1-42 and 1-40, but also with reduced 1-42/1-40 ratio with age. Amyloid deposition in plaques is accompanied by altered mitochondria and increased oxidative damage, post-translational modifications and accumulation of altered proteins at the dystrophic neurites surrounding plaques. Degradation pathways are also modified with disease progression including activation of the immunoproteasome together with variable alterations of the different protease activities of the ubiquitin-proteasome system. Present observations show modifications in the production of ß-amyloid and activation and malfunction of the subcellular degradation pathways that have general implications in the pathogenesis of AD and more particularly in specificities of FAD amyloidogenesis.