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martes, 7 de diciembre de 2010

Protective actions of sex steroid hormones in Alzheimer’s disease.

Héctor Lara-Tapia: Y en la andropausia?

Héctor, la pregunta no es simple de contestar, pero es muy interesante, pues a priori uno juzgaría que los estrógenos no tienen ningún papel en el hipocampo masculino, revisando la literatura me encuentro que hay producción local, es decir cerebral y especificamente hipocampal de estrógenos y que estos se producen o sintetizan activándose la aromatasa, lo curioso es que ésta se activa con el estímulo de la testosterona en el caso del hipocampo masculino, en otras palabras la testosterona induciría la producción de estradiol hipocampal...Lo que parece innegable es el efecto positivo del estradiol sobre la cognición, la neurogénesis y generación de espinas dendríticas.

Te anexo esto que me encontré y que resume el asunto de las hormonas y su efecto protectivo en la enfermedad de Alzheimer

Artículo completo:  AQUI

RESUMEN:
Protective actions of sex steroid hormones in 
Alzheimer’s disease
Christian J. Pike1,*, Jenna C. Carroll1,2, Emily R. Rosario1, and Anna Barron1
1Davis School of Gerontology, University of Southern California, Los Angeles, CA 90089 USA
2Neuroscience Graduate Program, University of Southern California, Los Angeles, CA 90089 USA
Abstract
Risk for Alzheimer’s disease (AD) is associated with age-related loss of sex steroid hormones in
both women and men. In postmenopausal women, the precipitous depletion of estrogens and
progestogens is hypothesized to increase susceptibility to AD pathogenesis, a concept largely
supported by epidemiological evidence but refuted by some clinical findings. Experimental evidence
suggests that estrogens have numerous neuroprotective actions relevant to prevention of AD, in
particular promotion of neuron viability and reduction of β-amyloid accumulation, a critical factor
in the initiation and progression of AD. Recent findings suggest neural responsiveness to estrogen
can diminish with age, reducing neuroprotective actions of estrogen and, consequently, potentially
limiting the utility of hormone therapies in aged women. In addition, estrogen neuroprotective actions
are also modulated by progestogens. Specifically, continuous progestogen exposure is associated
with inhibition of estrogen actions whereas cyclic delivery of progestogens may enhance neural
benefits of estrogen. In recent years, emerging literature has begun to elucidate a parallel relationship
of sex steroid hormones and AD risk in men. Normal age-related testosterone loss in men is associated
with increased risk to several diseases including AD. Like estrogen, testosterone has been established
as an endogenous neuroprotective factor that not only increases neuronal resilience against ADrelated
insults, but also reduces β- amyloid accumulation. Androgen neuroprotective effects are
mediated both directly by activation of androgen pathways and indirectly by aromatization to
estradiol and initiation of protective estrogen signaling mechanisms. The successful use of hormone
therapies in aging men and women to delay, prevent, and or treat AD will require additional research
to optimize key parameters of hormone therapy and may benefit from the continuing development
of selective estrogen and androgen receptor modulators.

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