Donación de órganos desde una perspectiva del personal médico / Organ donation from a personal physician perspective

Objetivo: Determinar los factores que dificultan el proceso de donación de órganos en el personal médico. Métodología: Se realizó una revisión sistemática para conocer los factores que han contribuido a las bajas tasas de donación de órganos, desde una perspectiva del personal médico. Se eligieron 28 artículos de revistas indexadas en Crossref, PubMed, Elsevier, Medline y Scielo, además de páginas oficiales. La búsqueda se realizó mediante palabras clave (Donación, Trasplante, Muerte encefálica y Personal Médico) en español e inglés. Resultados: Se revisaron 28 artículos indexados y paginas oficiales donde el desconocimiento del personal médico para identificar potenciales donadores y la legislación referente al tema, la falta de personal y organización médica, así como la actitud son factores que dificultan el proceso de donación de órganos. Conclusiones: Se requiere implementar estrategias para un mayor conocimiento del proceso de donación de órganos para el personal médico, además de capacitación organizacional y constante retroalimentación, de lo contario los resultados continuaran como no positivos.(AU)

Aim: Determine the factors that hinder the organ donation process in medical personnel. Methodology: A systematic review was conducted to discover the factors that have contributed to the low rates of organ donation, from the perspective of medical personnel. 28 articles from journals indexed in Crossref, PubMed, Elsevier, Medline and Scielo were selected, in addition to the official pages. The search was performed using keywords (donation, transplant, brain death and medical personnel) in spanish and english. Results: 28 indexed articles and official pages were reviewed where the ignorance of medical personnel to identify possible donors and related legislation, the lack of personnel, infrastructure and medical organization, as well as attitude are determining factors in the low donation of Organs. Conclusions: it is necessary to implement strategies for a better knowledge of the organ donation process for medical personnel, in addition to organizational training and constant feedback. otherwise the results will continue as non-positive.(AU)

Connecting Mind-Body Therapy-Mediated Effects to Pathological Features of Alzheimer's Disease.

Alzheimer's disease (AD) is a complex, multifactorial neurodegenerative disorder that represents a major and increasing global health challenge. In most cases, the first clinical symptoms of AD are preceded by neuropathological changes in the brain that develop years to decades before their onset. Therefore, research in the last years has focused on this preclinical stage of AD trying to discover intervention strategies that might, if implemented effectively, delay or prevent disease progression. Among those strategies, mind-body therapies such as yoga and meditation have gained increasing interest as complementary alternative interventions. Several studies have reported a positive impact of yoga and meditation on brain health in both healthy older adults and dementia patients. However, the underlying neurobiological mechanisms contributing to these effects are currently not known in detail. More specifically, it is not known whether yogic interventions, directly or indirectly, can modulate risk factors or pathological mechanisms involved in the development of dementia. In this article, we first review the literature on the effects of yogic practices on outcomes such as cognitive functioning and neuropsychiatric symptoms in patients with mild cognitive impairment and dementia. Then, we analyze how yogic interventions affect different risk factors as well as aspects of AD pathophysiology based on observations of studies in healthy individuals or subjects with other conditions than dementia. Finally, we integrate this evidence and propose possible mechanisms that might explain the positive effects of yogic interventions in cognitively impaired individuals.

Re-thinking the Etiological Framework of Neurodegeneration.

Neurodegenerative diseases are among the leading causes of disability and death worldwide. The disease-related socioeconomic burden is expected to increase with the steadily increasing life expectancy. In spite of decades of clinical and basic research, most strategies designed to manage degenerative brain diseases are palliative. This is not surprising as neurodegeneration progresses "silently" for decades before symptoms are noticed. Importantly, conceptual models with heuristic value used to study neurodegeneration have been constructed retrospectively, based on signs and symptoms already present in affected patients; a circumstance that may confound causes and consequences. Hence, innovative, paradigm-shifting views of the etiology of these diseases are necessary to enable their timely prevention and treatment. Here, we outline four alternative views, not mutually exclusive, on different etiological paths toward neurodegeneration. First, we propose neurodegeneration as being a secondary outcome of a primary cardiovascular cause with vascular pathology disrupting the vital homeostatic interactions between the vasculature and the brain, resulting in cognitive impairment, dementia, and cerebrovascular events such as stroke. Second, we suggest that the persistence of senescent cells in neuronal circuits may favor, together with systemic metabolic diseases, neurodegeneration to occur. Third, we argue that neurodegeneration may start in response to altered body and brain trophic interactions established via the hardwire that connects peripheral targets with central neuronal structures or by means of extracellular vesicle (EV)-mediated communication. Lastly, we elaborate on how lifespan body dysbiosis may be linked to the origin of neurodegeneration. We highlight the existence of bacterial products that modulate the gut-brain axis causing neuroinflammation and neuronal dysfunction. As a concluding section, we end by recommending research avenues to investigate these etiological paths in the future. We think that this requires an integrated, interdisciplinary conceptual research approach based on the investigation of the multimodal aspects of physiology and pathophysiology. It involves utilizing proper conceptual models, experimental animal units, and identifying currently unused opportunities derived from human data. Overall, the proposed etiological paths and experimental recommendations will be important guidelines for future cross-discipline research to overcome the translational roadblock and to develop causative treatments for neurodegenerative diseases.

Abeta targets of the biosimilar antibodies of Bapineuzumab, Crenezumab, Solanezumab in comparison to an antibody against N­truncated Abeta in sporadic Alzheimer disease cases and mouse models.

Solanezumab and Crenezumab are two humanized antibodies targeting Amyloid-ß (Aß) which are currently tested in multiple clinical trials for the prevention of Alzheimer's disease. However, there is a scientific discussion ongoing about the target engagement of these antibodies. Here, we report the immunohistochemical staining profiles of biosimilar antibodies of Solanezumab, Crenezumab and Bapineuzumab in human formalin-fixed, paraffin-embedded tissue and human fresh frozen tissue. Furthermore, we performed a direct comparative immunohistochemistry analysis of the biosimilar versions of the humanized antibodies in different mouse models including 5XFAD, Tg4-42, TBA42, APP/PS1KI, 3xTg. The staining pattern with these humanized antibodies revealed a surprisingly similar profile. All three antibodies detected plaques, cerebral amyloid angiopathy and intraneuronal Aß in a similar fashion. Remarkably, Solanezumab showed a strong binding affinity to plaques. We also reaffirmed that Bapineuzumab does not recognize N-truncated or modified Aß, while Solanezumab and Crenezumab do detect N-terminally modified Aß peptides Aß4-42 and pyroglutamate Aß3-42. In addition, we compared the results with the staining pattern of the mouse NT4X antibody that recognizes specifically Aß4-42 and pyroglutamate Aß3-42, but not full-length Aß1-42. In contrast to the biosimilar antibodies of Solanezumab, Crenezumab and Bapineuzumab, the murine NT4X antibody shows a unique target engagement. NT4X does barely cross-react with amyloid plaques in human tissue. It does, however, detect cerebral amyloid angiopathy in human tissue. In Alzheimer mouse models, NT4X detects intraneuronal Aß and plaques comparable to the humanized antibodies. In conclusion, the biosimilar antibodies Solanezumab, Crenezumab and Bapineuzumab strongly react with amyloid plaques, which are in contrast to the NT4X antibody that hardly recognizes plaques in human tissue. Therefore, NT4X is the first of a new class of therapeutic antibodies.