Roberta Diaz Brinton mainly investigates Estrogen, Internal medicine, Endocrinology, Neuroscience and Neuroprotection. Her research integrates issues of Neuron, Menopause, Anaerobic glycolysis, Estrogen receptor and Mitochondrion in her study of Estrogen. Her Neuron study incorporates themes from Agonist and Hippocampal formation.
Her research investigates the connection between Internal medicine and topics such as MAPK/ERK pathway that intersect with problems in Medroxyprogesterone acetate and Progestin. Her Cognition, Neurogenesis and Central nervous system study in the realm of Neuroscience interacts with subjects such as Context. Her biological study spans a wide range of topics, including Neuroactive steroid, Allopregnanolone, Neuroplasticity and Neural stem cell.
Her scientific interests lie mostly in Internal medicine, Endocrinology, Disease, Neuroscience and Estrogen. When carried out as part of a general Internal medicine research project, her work on Neuroprotection and Alzheimer's disease is frequently linked to work in Reproductive senescence, therefore connecting diverse disciplines of study. Her research in Endocrinology tackles topics such as Mitochondrion which are related to areas like Oxidative stress.
Her Disease research focuses on Allopregnanolone and how it relates to Pharmacokinetics. Her Neuroscience research incorporates elements of Long-term potentiation and Vasopressin. Her study on Estrogen also encompasses disciplines like
Roberta Diaz Brinton focuses on Disease, Internal medicine, Dementia, Cognition and Oncology. Her Disease research is multidisciplinary, relying on both Verbal memory, Neuroscience, Cohort and Allopregnanolone. Her studies in Internal medicine integrate themes in fields like Endocrinology and Cardiology.
Her research in Endocrinology intersects with topics in Bioenergetics and Intima-media thickness. Her Dementia research includes elements of Progestin, Hormone therapy and Observational study. The study incorporates disciplines such as Inflammatory biomarkers, Menopause, Estrogen and Cognitive decline in addition to Oncology.
Internal medicine, Disease, Menopause, Mitochondrion and Oncology are her primary areas of study. Roberta Diaz Brinton conducts interdisciplinary study in the fields of Internal medicine and Epigenomics through her works. Her work deals with themes such as Metabolome, Precision medicine, Physiology and Pathogenesis, which intersect with Disease.
Her Menopause study integrates concerns from other disciplines, such as Gerontology, Diabetes mellitus, Immune system, Hormone and Estrogen. Her biological study deals with issues like Genetic risk, which deal with fields such as Neuroscience. Her Mitochondrion research includes themes of Matrix and Cytosol.
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Mitochondrial bioenergetic deficit precedes Alzheimer's pathology in female mouse model of Alzheimer's disease
Jia Yao;Ronald W. Irwin;Liqin Zhao;Jon Nilsen.
Proceedings of the National Academy of Sciences of the United States of America (2009)
17β-Estradiol Enhances NMDA Receptor-Mediated EPSPs and Long-Term Potentiation
M. R. Foy;J. Xu;X. Xie;R. D. Brinton.
Journal of Neurophysiology (1999)
Progesterone Receptors: Form and Function in Brain
Roberta Diaz Brinton;Richard F. Thompson;Michael R. Foy;Michel Baudry.
Frontiers in Neuroendocrinology (2008)
Impact of progestins on estrogen-induced neuroprotection: Synergy by progesterone and 19-norprogesterone and antagonism by medroxyprogesterone acetate
Jon Nilsen;Roberta Diaz Brinton.
Endocrinology (2002)
Estrogen, Menopause, and the Aging Brain: How Basic Neuroscience Can Inform Hormone Therapy in Women
John H Morrison;Roberta D Brinton;Peter J Schmidt;Andrea C Gore.
The Journal of Neuroscience (2006)
Estrogen: a master regulator of bioenergetic systems in the brain and body.
Jamaica R Rettberg;Jia Yao;Roberta Diaz Brinton.
Frontiers in Neuroendocrinology (2014)
Age, APOE and sex: Triad of risk of Alzheimer's disease.
Brandalyn C. Riedel;Paul M. Thompson;Roberta Diaz Brinton.
The Journal of Steroid Biochemistry and Molecular Biology (2016)
17β-estradiol induced Ca2+ influx via L-type calcium channels activates the Src/ERK/cyclic-AMP response element binding protein signal pathway and BCL-2 expression in rat hippocampal neurons: A potential initiation mechanism for estrogen-induced neuroprotection
T.-W. Wu;J.M. Wang;S. Chen;R.D. Brinton.
Neuroscience (2005)
Mechanism of estrogen-mediated neuroprotection: regulation of mitochondrial calcium and Bcl-2 expression.
Jon Nilsen;Roberta Diaz Brinton.
Proceedings of the National Academy of Sciences of the United States of America (2003)
The healthy cell bias of estrogen action: mitochondrial bioenergetics and neurological implications.
Roberta Diaz Brinton.
Trends in Neurosciences (2008)
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