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PD AND HORMONES PART SIX
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a brief selection from Medscape/Medline on line:
http://www5.medscape.com/default.mhtml

-----32---------------------------------------------------------------------
Title: Hormones and Parkinson's disease [letter; comment]
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Title Abreviation: Neurology
Date of Pub: 1995 May
Author: Giladi N; Honigman S;
Issue/Part/Supplement: 5
Volume Issue: 45
Pagination: 1028-9
MESH Headings: Case Report; Female; Hormones (*PH); Human; Levodopa (TU);
Menstrual Cycle (*PH); Middle Age; Parkinson Disease (DT/*PP); -RN-;
Journal Title Code: NZ0
Publication Type: COMMENT
Date of Entry: 950615N
Entry Month: 9508
Country: UNITED STATES
Index Priority: 1
Language: Eng
Unique Identifier: 95265174
ISSN: 0028-3878
Last Revision Date: 950807

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Title: Neuroleptic malignant syndrome in a parkinsonian woman during the
premenstrual period
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[see comments]
Title Abreviation: Neurology
Date of Pub: 1993 May
Author: Mizuta E; Yamasaki S; Nakatake M; Kuno S;
Issue/Part/Supplement: 5
Volume Issue: 43
Pagination: 1048-9
MESH Headings: Body Temperature; Carbidopa (*TU); Case Report; Drug
Combinations; Female; Human; Levodopa (*TU); Menstrual Cycle (*); Middle Age;
Neuroleptic Malignant  Syndrome (ET/*PP); Parkinson Disease (CO/DT/*PP); -RN-;
Journal Title Code: NZ0
Publication Type: JOURNAL ARTICLE
Date of Entry: 930611N
Entry Month: 9308
Country: UNITED STATES
Index Priority: 1
Language: Eng
Unique Identifier: 93261586
ISSN: 0028-3878

Abstract: A 45-year-old woman with Parkinson's disease developed neuroleptic
malignant syndrome (NMS) despite lack of levodopa withdrawal. She experienced
two episodes characterized by indomethacin-resistant hyperthermia,
hyperhidrosis, and aggravation of parkinsonism. The symptoms, however,
disappeared during menstruation. We suggest that the development of NMS may
depend, in part, upon the hormonal state.

Abstract By: Author
Address: Department of Neurology, Utano National Hospital, Kyoto, Japan.
Last Revision Date: 950807

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Title: Acetazolamide therapy of menstrual-related fluctuations in Parkinson's
disease.
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Title Abreviation: Mov Disord
Date of Pub: 1993 Apr
Author: Factor SA;
Issue/Part/Supplement: 2
Volume Issue: 8
Pagination: 240-1
MESH Headings: Acetazolamide (*AD); Adult; Carbidopa (AD/AE); Case Report; Drug
Administration Schedule; Drug Therapy, Combination; Female; Human; Levodopa
(AD/AE); Menstruation Disorders (*DT); Neurologic Examination (DE); Parkinson
Disease (*DT); Support, Non-U.S. Gov't; -RN-;
Journal Title Code: NIA
Publication Type: JOURNAL ARTICLE
Date of Entry: 930518N
Entry Month: 9307
Country: UNITED STATES
Index Priority: 2
Language: Eng
Unique Identifier: 93233716
ISSN: 0855-3185
Address: Department of Neurology, Albany Medical College, New York.

-----35---------------------------------------------------------------------
Title: Estrogens and Parkinson's disease.
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Title Abreviation: Med Hypotheses
Date of Pub: 1994 Apr
Author: Session DR; Pearlstone MM; Jewelewicz R; Kelly AC;
Issue/Part/Supplement: 4
Volume Issue: 42
Pagination: 280-2
MESH Headings: Adult; Case Report; Estrogens (*PH); Female; Human; Leuprolide
(AD); Parkinson Disease (*PP/TH); Premenopause (DE); -RN-;
Journal Title Code: M0M
Publication Type: JOURNAL ARTICLE
Date of Entry: 940926N
Entry Month: 9412
Country: ENGLAND
Index Priority: 2
Language: Eng
Unique Identifier: 94352251
ISSN: 0306-9877

Abstract: There is substantial evidence that estrogens modulate the activity of
dopamine in the extrapyramidal system. However, there is conflicting data as to
the exact mechanism of estrogen's effects. The majority of clinical reports
support an antidopaminergic effect of estrogens on Parkinsonian symptoms.
Generally, Parkinsonism worsens with estrogen therapy. We report a case of
improvement in Parkinsonian symptoms in a premenopausal patient when placed on
leuprolide acetate. The pharmacologic menopause induced by leuprolide acetate
leads to a hypoestrogenic state. We hypothesize that the decrease in estrogen
improves Parkinson's disease symptoms via the relief of its antidopaminergic
effects on the nigrostriatal pathway.

Abstract By: Author
Address: Department of Obstetrics and Gynecology, Columbia-Presbyterian Medical
Center, New York, New York 10032.

-----36---------------------------------------------------------------------
Title: The growth inhibitory properties of a dopamine agonist (SKF 38393) on
MCF-7 cells.
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Title Abreviation: Anticancer Drugs
Date of Pub: 1995 Jun
Author: Johnson DE; Ochieng J; Evans SL;
Issue/Part/Supplement: 3
Volume Issue: 6
Pagination: 471-4
MESH Headings: Breast Neoplasms (*DT/ME); Cell Division (DE); Dopamine Agonists
(*PD); Estradiol (PD); Haloperidol (PD); Human; Prolactin (ME); Receptors,
Estrogen (DE/ME); Support, U.S. Gov't, P.H.S.; SK&F-38393 (*PD); Tamoxifen (PD);
Tumor Cells, Cultured; -RN-;  Journal Title Code: A9F
Publication Type: JOURNAL ARTICLE
Date of Entry: 951017N
Entry Month: 9512
Country: ENGLAND
Index Priority: 2
Language: Eng
Unique Identifier: 95399823
ISSN: 0959-4973

Abstract: Dopamine agonists have been indicated as treatment for disorders such
as Parkinson's disease, cardiogenic shock and dopamine insufficiency. A unique
relationship exists between dopamine and carcinogenicity. Chronic prolactin
stimulation has been identified as a promoter of carcinogenicity. Prolactin
secretion is regulated through dopamine receptor activation. Dopaminergic
agonists inhibit prolactin release and antagonists increase release. High levels
of prolactin have been shown to suppress production of estrogen and
progesterone. As a result of these findings, a series of experiments were
designed to examine the effects of a specific dopamine agonist, SKF 38393,
against MCF-7 cells. MDA-MB231 and MCF-10 cells were used as negative controls.
The breast cancer in vitro screening procedure involved the plating of MCF-7,
MDA-MB231 and MCF-10 cells in a 96-well plate assay. After 1 day, the cells were
exposed to SKF 38393 for 2 days and cell growth was determined by the Alamar
blue dye reagent method. The optical density data was analyzed and IC50 values
determined. The results indicated that SKF 38393 caused a significant decrease
in proliferation of MCF-7 cells. The IC50 value was 0.1 +/- 0.03 microM. The
results also indicated no significant effect on MDA-MB231 and MCF-10 cells.

Abstract By: Author
Address: Department of Pharmacology, Meharry Medical College, Nashville, TN
37208, USA.

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Title: Sex differences and effects of estrogen on dopamine and DOPAC release
from the striatum of male and female CD-1 mice.
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Title Abreviation: Exp Neurol
Date of Pub: 1994 Feb
Author: McDermott JL; Liu B; Dluzen DE;
Issue/Part/Supplement: 2
Volume Issue: 125
Pagination: 306-11
MESH Headings: Animal; Corpus Striatum (*ME); Dopamine (*ME); Estrogens (*PD);
Female; Male; Mice; Potassium (PD); Sex Characteristics (*); Substantia Nigra
(ME); 3,4-Dihydroxyphenylacetic Acid (*ME);  Journal Title Code: EQF
Publication Type: JOURNAL ARTICLE
Date of Entry: 940323N
Entry Month: 9405
Country: UNITED STATES
Index Priority: 1
Language: Eng
Unique Identifier: 94148054
ISSN: 0014-4886

Abstract: In the present study, we directly compare striatal dopamine metabolism
in gonadectomized male and female CD-1 mice treated with 2 days of estrogen or
oil vehicle. Basal and potassium-stimulated dopamine and 4-dihydroxyphenylacetic
acid (DOPAC) release from in vitro superfused striatum as well as pre- and
postsuperfusion tissue dopamine contents were measured. Both basal and
potassium-stimulated dopamine release were significantly higher and DOPAC
release was significantly lower in males than in females. However, striatal
tissue dopamine content was lower in males than in females. Estrogen-treated
female mice showed increased basal and potassium-stimulated dopamine release
compared to oil-treated females without affecting tissue dopamine content.
Estrogen did not affect striatal dopamine concentrations or release in males.
These results demonstrate clear sex differences in striatal dopamine turnover
and concentrations under conditions of equal hormonal status. The results also
indicate that estrogen can exert substantial effects on striatal dopamine
metabolism by acting specifically in females to increase neuronal dopamine
synthesis and release without depleting dopamine content. These results have
important implications for the observed sex differences in clinical movement
disorders such as Parkinson's disease.

Abstract By: Author
Address: Department of Medicine, Case Western Reserve University, Cleveland,
Ohio 44106.

-----38---------------------------------------------------------------------
Title: Sexual differences in sensitivity to methamphetamine toxicity.
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Title Abreviation: J Neural Transm Gen Sect
Date of Pub: 1993
Author: Wagner GC; Tekirian TL; Cheo CT;
Issue/Part/Supplement: 1
Volume Issue: 93
Pagination: 67-70
MESH Headings: Animal; Corpus Striatum (ME); Dopamine (ME); Female; Male;
Methamphetamine (*TO); Mice; Mice, Inbred Strains; Nervous System (*DE); Sex
Characteristics (*); -RN-;  Journal Title Code: AJ2
Publication Type: JOURNAL ARTICLE
Date of Entry: 931020N
Entry Month: 9312
Country: AUSTRIA
Index Priority: 2
Language: Eng
Unique Identifier: 93384770
Unique Identifier: 93384770
SSN: -HEADING-

Abstract: Male and female mice were treated with methamphetamine (10.0
mg/kg/injection for four injections) and sacrificed two weeks later. It was
observed that the methamphetamine treatment caused depletions in striatal
dopamine which were significantly greater in males (74%) than in females (56%).
These results indicate that estrogen may have a protective effect against
methamphetamine-induced dopamine depletions and may relate to the fact that
males are more likely to incur Parkinson's disease than females.

Abstract By: Author
Address: Department of Psychology, Rutgers University, New Brunswick, NJ.

-----39---------------------------------------------------------------------
Title: Sarcopenia in aging humans: the impact of menopause and disease.
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Title Abreviation: J Gerontol A Biol Sci Med Sci
Date of Pub: 1995 Nov
Author: Poehlman ET; Toth MJ; Fishman PS; Vaitkevicius P; Gottlieb SS; Fisher
ML; Fonong T;
Issue/Part/Supplement: -HEADING-
Volume Issue: 50
Spec No Pagination: 73-7
MESH Headings: Adipose Tissue (ME/PP); Aged; Aged, 80 and over; Aging (ME/*PH);
Body Composition (*PH); Case-Control Studies; Disease (*); Energy Metabolism;
Female; Heart Failure, Congestive (CO/ME/PP); Human; Menopause (ME/*PH); Middle
Age; Muscle, Skeletal (ME/*PP); Muscular Atrophy (ET); Parkinson Disease
(CO/ME/PP); Support, U.S. Gov't, P.H.S.; Weight Loss; -AA-;  Journal Title Code:
CBA
Publication Type: JOURNAL ARTICLE
Date of Entry: 960111N
Entry Month: 9603
Country: UNITED STATES
Index Priority: 1
Language: Eng
Unique Identifier: 96067374
ISSN: 1079-5006

Abstract: We examine the association of the menopause transition, congestive
heart failure, and Parkinson's disease on body composition and energy
expenditure. We present evidence suggesting that the normal menopausal
transition is associated with accelerated loss of fat-free mass, a decline in
resting metabolic rate, and increased central body fatness. Second, we show that
the cardiac cachexia associated with heart failure is partially due to an
levated level of energy expenditure. Despite having a lower quantity of fat-free
mass, congestive heart failure patients have a higher resting metabolic rate
approximately 283 kcal/d) for their metabolic size than healthy elderly. The
elevated level of resting energy expenditure probably contributes to their
unexplained weight loss. Parkinson's patients experience muscular rigidity and
tremor which could contribute to inappropriately high levels of energy
expenditure and difficulty in maintaining body weight and composition. We
examined resting metabolic rate and body composition in eight Parkinson's
patients and 34 healthy age-matched controls. Parkinson's patients showed lower
levels of fat-free mass (approximately 6 kg), but similar resting metabolic
rates (1601 +/- 250 kcal/d) versus healthy controls (1671 +/- 212 kcal/d),
suggesting a hypermetabolic state. A re-examination of daily energy needs and
the metabolic factors contributing to periods of energy imbalance during the
menopausal transition and in several disease states may be a prerequisite to
offsetting accelerated sarcopenia.

Abstract By: Author
Address: Department of Medicine, GRECC, Baltimore VA Medical Center, University
of Maryland, USA.
Number of References: 25

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