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Book ; Online: Geriatrics

Atwood, Craig S.

2012

Keywords	Geriatric medicine
Size	1 electronic resource (248 pages)
Publisher	IntechOpen
Document type	Book ; Online
Note	English ; Open Access
HBZ-ID	HT021049737
ISBN	9789535168256 ; 9535168258
Database	ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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Book ; Online: Pluripotent Stem Cell Biology : Advances in Mechanisms, Methods and Models

Atwood, Craig S. / Vadakkadath Meethal, Sivan

2014

Keywords	Proteins ; Cellular biology (cytology)
Size	1 electronic resource (242 pages)
Publisher	IntechOpen
Document type	Book ; Online
Note	English ; Open Access
HBZ-ID	HT021050302
ISBN	9789535172130 ; 9535172131
Database	ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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Article ; Online: Playing Russian Roulette with Alzheimer's Disease Patients: Do the Cognitive Benefits of Lecanemab Outweigh the Risk of Edema, Stroke and Encephalitis?

Atwood, Craig S / Perry, George

Journal of Alzheimer's disease : JAD

2023 Volume 92, Issue 3, Page(s) 799–801

Abstract: The questionable approval of aducanumab and the recent approval of lecanemab (Leqembi; Eisai and Biogen) by the FDA has raised the issue of safety (stroke, meningitis, and encephalitis) over efficacy (slowing of cognitive decline). This communication ... ...

Abstract	The questionable approval of aducanumab and the recent approval of lecanemab (Leqembi; Eisai and Biogen) by the FDA has raised the issue of safety (stroke, meningitis, and encephalitis) over efficacy (slowing of cognitive decline). This communication recounts the important physiological functions of amyloid-β as a barrier protein with unique sealant and anti-pathogenic activities important for maintaining vascular integrity coupled with innate immune functions that prevent encephalitis and meningitis. The approval of a drug that obviates both of these purposive functions increases the risk of hemorrhage, edema and downstream pathogenic outcomes and should be clearly outlined to patients.
MeSH term(s)	Humans ; Alzheimer Disease/metabolism ; Amyloid beta-Peptides/metabolism ; Stroke ; Encephalitis ; Cognition ; Edema ; Russia
Chemical Substances	lecanemab (12PYH0FTU9) ; Amyloid beta-Peptides
Language	English
Publishing date	2023-02-27
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	1440127-7
ISSN	1875-8908 ; 1387-2877
ISSN (online)	1875-8908
ISSN	1387-2877
DOI	10.3233/JAD-230040
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Article: Estropause, Sex Hormones and Metal Homeostasis in the Mouse Brain.

Liu, Tianbing / Bowen, Richard L / Wilson, Andrea C / Atwood, Craig S

Frontiers in neurology

2022 Volume 13, Page(s) 841822

Abstract: Alterations in brain metal ion homeostasis have been reported with aging and are implicated in the pathogenesis of neurodegenerative diseases. To assess whether age-related changes in hypothalamic-pituitary-gonadal (HPG) hormones might be involved in ... ...

Abstract	Alterations in brain metal ion homeostasis have been reported with aging and are implicated in the pathogenesis of neurodegenerative diseases. To assess whether age-related changes in hypothalamic-pituitary-gonadal (HPG) hormones might be involved in modulating brain metal ion homeostasis, we treated 7.5-month intact, sham-ovariecomized and ovariectomized C57B6SJL mice with vehicle or leuprolide acetate (for 9-months) to differentiate between whether sex steroids or gonadotropins might modulate brain metal ion concentrations. Unlike other aging mammals, there was no increase in plasma luteinizing hormone (LH) and follicle-stimulating hormone (FSH) concentrations following estropause in mice, suggesting there was sufficient residual production by the follicle depleted ovary, of sex steroids like estrogens and protein hormones like the inhibins, in order to suppress pituitary LH/FSH production. Castration on the other hand induced significant increases in circulating LH and FSH. Modulation of plasma sex steroid and gonadotropin levels did not significantly alter the concentrations of brain metals tested (Fe, Zn, Cu, Mn, Co, Ni, Al, Li), although there was a tendency for a decrease in all brain metals following ovariectomy (low estrogens and progesterone, high gonadotropins), a response that was reversed with leuprolide acetate treatment (low sex steroids, low gonadotropins). Brain Cu concentration was the only metal correlated with plasma LH (-0.37,
Language	English
Publishing date	2022-05-11
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2564214-5
ISSN	1664-2295
ISSN	1664-2295
DOI	10.3389/fneur.2022.841822
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Human versus non-human sex steroid use in hormone replacement therapies part 1: Preclinical data.

Atwood, Craig S / Ekstein, Samuel F

Molecular and cellular endocrinology

2018 Volume 480, Page(s) 12–35

Abstract: Prior to 2002, hormone replacement therapy (HRT) was considered to be an important component of postmenopausal healthcare. This was based on a plethora of basic, epidemiological and clinical studies demonstrating the health benefits of supplementation ... ...

Abstract	Prior to 2002, hormone replacement therapy (HRT) was considered to be an important component of postmenopausal healthcare. This was based on a plethora of basic, epidemiological and clinical studies demonstrating the health benefits of supplementation with human sex steroids. However, adverse findings from the Women's Health Initiative (WHI) studies that examined the 2 major forms of HRT in use in the US at that time - Premarin (conjugated equine estrogens; CEE) and Prempro (CEE + medroxyprogesterone acetate; MPA), cast a shadow over the use of any form of HRT. Here we review the biochemical and physiological differences between the non-human WHI study hormones - CEE and MPA, and their respective human counterparts 17β-estradiol (E
MeSH term(s)	Animals ; Drug Combinations ; Estradiol/chemistry ; Estradiol/therapeutic use ; Estrogens, Conjugated (USP)/chemistry ; Estrogens, Conjugated (USP)/therapeutic use ; Gonadal Steroid Hormones/chemistry ; Gonadal Steroid Hormones/therapeutic use ; Hormone Replacement Therapy ; Humans ; Medroxyprogesterone Acetate/chemistry ; Medroxyprogesterone Acetate/therapeutic use ; Progesterone/chemistry
Chemical Substances	Drug Combinations ; Estrogens, Conjugated (USP) ; Gonadal Steroid Hormones ; Prempro ; Progesterone (4G7DS2Q64Y) ; Estradiol (4TI98Z838E) ; Medroxyprogesterone Acetate (C2QI4IOI2G)
Language	English
Publishing date	2018-10-09
Publishing country	Ireland
Document type	Journal Article ; Review
ZDB-ID	187438-x
ISSN	1872-8057 ; 0303-7207
ISSN (online)	1872-8057
ISSN	0303-7207
DOI	10.1016/j.mce.2018.10.003
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Article ; Online: Septal hypertrophy and cell cycle re-entry in AD.

Butler, Tracy / Bowen, Richard / Atwood, Craig S

Aging

2019 Volume 11, Issue 2, Page(s) 297–298

MeSH term(s)	Alzheimer Disease/diagnosis ; Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Basal Forebrain ; Cell Cycle/physiology ; Humans ; Septal Nuclei/cytology
Language	English
Publishing date	2019-01-22
Publishing country	United States
Document type	Editorial ; Research Support, N.I.H., Extramural
ISSN	1945-4589
ISSN (online)	1945-4589
DOI	10.18632/aging.101777
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Human versus non-human sex steroid use in hormone replacement therapies part 1: Preclinical data

Atwood, Craig S / Samuel F. Ekstein

Molecular and cellular endocrinology. 2019 Jan. 15, v. 480

2019

Abstract	Prior to 2002, hormone replacement therapy (HRT) was considered to be an important component of postmenopausal healthcare. This was based on a plethora of basic, epidemiological and clinical studies demonstrating the health benefits of supplementation with human sex steroids. However, adverse findings from the Women's Health Initiative (WHI) studies that examined the 2 major forms of HRT in use in the US at that time - Premarin (conjugated equine estrogens; CEE) and Prempro (CEE + medroxyprogesterone acetate; MPA), cast a shadow over the use of any form of HRT. Here we review the biochemical and physiological differences between the non-human WHI study hormones – CEE and MPA, and their respective human counterparts 17β-estradiol (E2) and progesterone (P4). Preclinical data from the last 30 years demonstrate clear differences between human and non-human sex steroids on numerous molecular, physiological and functional parameters in brain, heart and reproductive tissue. In contrast to CEE supplementation, which is not always detrimental although certainly not as optimal as E2 supplementation, MPA is clearly not equivalent to P4, having detrimental effects on cognitive, cardiac and reproductive function. Moreover, unlike P4, MPA is clearly antagonistic of the positive effects of E2 and CEE on tissue function. These data indicate that minor chemical changes to human sex steroids result in physiologically distinct actions that are not optimal for tissue health and functioning.
Keywords	acetates ; brain ; clinical trials ; cognition ; estradiol ; health services ; heart ; hormone replacement therapy ; horses ; humans ; medroxyprogesterone ; postmenopause ; progesterone ; steroid hormones ; women's health ; United States
Language	English
Dates of publication	2019-0115
Size	p. 12-35.
Publishing place	Elsevier B.V.
Document type	Article
ZDB-ID	187438-x
ISSN	1872-8057 ; 0303-7207
ISSN (online)	1872-8057
ISSN	0303-7207
DOI	10.1016/j.mce.2018.10.003
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: A Unified Hypothesis of Early- and Late-Onset Alzheimer's Disease Pathogenesis.

Atwood, Craig S / Bowen, Richard L

Journal of Alzheimer's disease : JAD

2015 Volume 47, Issue 1, Page(s) 33–47

Abstract: Early-onset familial Alzheimer's disease (EOFAD) and late-onset sporadic AD (LOSAD) both follow a similar pathological and biochemical course that includes: neuron and synapse loss and dysfunction, microvascular damage, microgliosis, extracellular ... ...

Abstract	Early-onset familial Alzheimer's disease (EOFAD) and late-onset sporadic AD (LOSAD) both follow a similar pathological and biochemical course that includes: neuron and synapse loss and dysfunction, microvascular damage, microgliosis, extracellular amyloid-β deposition, tau phosphorylation, formation of intracellular neurofibrillary tangles, endoreduplication and related cell cycle events in affected brain regions. Any mechanistic explanation of AD must accommodate these biochemical and neuropathological features for both forms of the disease. In this insight paper we provide a unifying hypothesis for EOFAD and LOSAD that proposes that the aberrant re-entry of terminally differentiated, post-mitotic neurons into the cell division cycle is a common pathway that explains both early and late-onset forms of AD. Cell cycle abnormalities appear very early in the disease process, prior to the appearance of plaques and tangles, and explain the biochemical (e.g. tau phosphorylation), neuropathological (e.g. neuron hypertrophy; polypoidy) and cognitive changes observed in EOFAD and LOSAD. Genetic mutations in AβPP, PSEN1, and PSEN2 that alter amyloid-β precursor protein and Notch processing drive reactivation of the cell cycle in EOFAD, while age-related reproductive endocrine dyscrasia that upregulates mitogenic TNF signaling and AβPP processing toward the amyloidogenic pathway drives reactivation of the cell cycle in LOSAD. In essence, AβPP and presenilin mutations initiate early, what endocrine dyscrasia initiates later: aberrant cell cycle re-entry of post-mitotic neurons leading to neurodegeneration and cognitive decline in AD. Inhibition of cell cycle re-entry in post-mitotic neurons may be a useful therapeutic strategy to prevent, slow or halt disease progression.
MeSH term(s)	Alzheimer Disease/complications ; Alzheimer Disease/genetics ; Alzheimer Disease/pathology ; Amyloid beta-Protein Precursor/genetics ; Cell Cycle/genetics ; Humans ; Memory Disorders/etiology ; Memory Disorders/genetics ; Mutation/genetics ; Neurofibrillary Tangles/pathology ; Neurons/physiology ; Phosphorylation/genetics ; Presenilin-1/genetics
Chemical Substances	Amyloid beta-Protein Precursor ; Presenilin-1
Language	English
Publishing date	2015
Publishing country	Netherlands
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	1440127-7
ISSN	1875-8908 ; 1387-2877
ISSN (online)	1875-8908
ISSN	1387-2877
DOI	10.3233/JAD-143210
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: The endocrine dyscrasia that accompanies menopause and andropause induces aberrant cell cycle signaling that triggers re-entry of post-mitotic neurons into the cell cycle, neurodysfunction, neurodegeneration and cognitive disease.

Atwood, Craig S / Bowen, Richard L

Hormones and behavior

2015 Volume 76, Page(s) 63–80

Abstract: This article is part of a Special Issue "SBN 2014". Sex hormones are physiological factors that promote neurogenesis during embryonic and fetal development. During childhood and adulthood these hormones support the maintenance of brain structure and ... ...

Abstract	This article is part of a Special Issue "SBN 2014". Sex hormones are physiological factors that promote neurogenesis during embryonic and fetal development. During childhood and adulthood these hormones support the maintenance of brain structure and function via neurogenesis and the formation of dendritic spines, axons and synapses required for the capture, processing and retrieval of information (memories). Not surprisingly, changes in these reproductive hormones that occur with menopause and during andropause are strongly correlated with neurodegeneration and cognitive decline. In this connection, much evidence now indicates that Alzheimer's disease (AD) involves aberrant re-entry of post-mitotic neurons into the cell cycle. Cell cycle abnormalities appear very early in the disease, prior to the appearance of plaques and tangles, and explain the biochemical, neuropathological and cognitive changes observed with disease progression. Intriguingly, a recent animal study has demonstrated that induction of adult neurogenesis results in the loss of previously encoded memories while decreasing neurogenesis after memory formation during infancy mitigated forgetting. Here we review the biochemical, epidemiological and clinical evidence that alterations in sex hormone signaling associated with menopause and andropause drive the aberrant re-entry of post-mitotic neurons into an abortive cell cycle that leads to neurite retraction, neuron dysfunction and neuron death. When the reproductive axis is in balance, gonadotropins such as luteinizing hormone (LH), and its fetal homolog, human chorionic gonadotropin (hCG), promote pluripotent human and totipotent murine embryonic stem cell and neuron proliferation. However, strong evidence supports menopausal/andropausal elevations in the LH:sex steroid ratio as driving aberrant mitotic events. These include the upregulation of tumor necrosis factor; amyloid-β precursor protein processing towards the production of mitogenic Aβ; and the activation of Cdk5, a key regulator of cell cycle progression and tau phosphorylation (a cardinal feature of both neurogenesis and neurodegeneration). Cognitive and biochemical studies confirm the negative consequences of a high LH:sex steroid ratio on dendritic spine density and human cognitive performance. Prospective epidemiological and clinical evidence in humans supports the premise that rebalancing the ratio of circulating gonadotropins:sex steroids reduces the incidence of AD. Together, these data support endocrine dyscrasia and the subsequent loss of cell cycle control as an important etiological event in the development of neurodegenerative diseases including AD, stroke and Parkinson's disease.
MeSH term(s)	Andropause/physiology ; Animals ; Cell Cycle/physiology ; Cognition Disorders/metabolism ; Humans ; Menopause/metabolism ; Neurodegenerative Diseases/metabolism ; Neurons/metabolism ; Signal Transduction/physiology
Language	English
Publishing date	2015-07-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	214409-8
ISSN	1095-6867 ; 0018-506X
ISSN (online)	1095-6867
ISSN	0018-506X
DOI	10.1016/j.yhbeh.2015.06.021
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Article ; Online: Development of Classification Models for the Prediction of Alzheimer's Disease Utilizing Circulating Sex Hormone Ratios.

Hayashi, Kentaro / Gonzales, Tina K / Kapoor, Amita / Ziegler, Toni E / Meethal, Sivan Vadakkadath / Atwood, Craig S

Journal of Alzheimer's disease : JAD

2020 Volume 76, Issue 3, Page(s) 1029–1046

Abstract: Background: While sex hormones are essential for normal cognitive health, those individuals with greater endocrine dyscrasia around menopause and with andropause are more likely to develop cognitive loss and Alzheimer's disease (AD).: Objective: To ... ...

Abstract	Background: While sex hormones are essential for normal cognitive health, those individuals with greater endocrine dyscrasia around menopause and with andropause are more likely to develop cognitive loss and Alzheimer's disease (AD). Objective: To assess whether circulating sex hormones may provide an etiologically significant, surrogate biomarker, for cognitive decline. Methods: Plasma (n = 152) and serum (n = 107) samples from age- and gender-matched AD and control subjects from the Wisconsin Alzheimer's Disease Research Center (ADRC) were analyzed for 11 steroids and follicle-stimulating hormone. Logistic regression (LR), correlation analyses, and recursive partitioning (RP) were used to examine the interactions of hormones and hormone ratios and their association with AD. Models generated were then tested on an additional 43 ADRC samples. Results: The wide variation and substantial overlap in the concentrations of all circulating sex steroids across control and AD groups precluded their use for predicting AD. Classification tree analyses (RP) revealed interactions among single hormones and hormone ratios that associated with AD status, the most predictive including only the hormone ratios identified by LR. The strongest associations were observed between cortisol, cortisone, and androstenedione with AD, with contributions from progesterone and 17β-estradiol. Utilizing this model, we correctly predicted 81% of AD test cases and 64% of control test cases. Conclusion: We have developed a diagnostic model for AD, the Wisconsin Hormone Algorithm Test for Cognition (WHAT-Cog), that utilizes classification tree analyses of hormone ratios. Further refinement of this technology could provide a quick and cheap diagnostic method for screening those with AD.
MeSH term(s)	Aged ; Aged, 80 and over ; Alzheimer Disease/diagnosis ; Alzheimer Disease/psychology ; Biomarkers/blood ; Cognition/physiology ; Cognitive Dysfunction/diagnosis ; Cognitive Dysfunction/psychology ; Estradiol/metabolism ; Female ; Gonadal Steroid Hormones/metabolism ; Humans ; Male ; Predictive Value of Tests ; Testosterone/blood
Chemical Substances	Biomarkers ; Gonadal Steroid Hormones ; Testosterone (3XMK78S47O) ; Estradiol (4TI98Z838E)
Language	English
Publishing date	2020-07-03
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	1440127-7
ISSN	1875-8908 ; 1387-2877
ISSN (online)	1875-8908
ISSN	1387-2877
DOI	10.3233/JAD-200418
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