Neurotransmitter Dysfunction and Neurotransmitter Replacement Therapy as Part of Frontotemporal Dementia Treatment

2005 ◽  
Vol 1 (3) ◽  
pp. 345-351 ◽  
Author(s):  
Martine Vercelletto ◽  
Michel Bourin ◽  
Lucette Lacomblez ◽  
Patrice Verpillat ◽  
Pascal Derkinderen
2008 ◽  
Vol 4 ◽  
pp. T501-T501
Author(s):  
◽  
Bernd Ibach ◽  
Hans Gutzmann ◽  
Stefan Poljanski ◽  
Winfried Barta ◽  
...  

Brain ◽  
2020 ◽  
Vol 143 (6) ◽  
pp. 1628-1631
Author(s):  
James J Doyle ◽  
J Alex Parker ◽  
Andrew Bateman

This scientific commentary refers to ‘Loss of TMEM106B leads to myelination deficits: implications for frontotemporal dementia treatment strategies’, by Zhou et al. (doi:10.1093/brain/awaa141).


2012 ◽  
Vol 2012 ◽  
pp. 1-18 ◽  
Author(s):  
Richelin V. Dye ◽  
Karen J. Miller ◽  
Elyse J. Singer ◽  
Andrew J. Levine

Over the past two decades, there has been a significant amount of research investigating the risks and benefits of hormone replacement therapy (HRT) with regards to neurodegenerative disease. Here, we review basic science studies, randomized clinical trials, and epidemiological studies, and discuss the putative neuroprotective effects of HRT in the context of Alzheimer’s disease, Parkinson’s disease, frontotemporal dementia, and HIV-associated neurocognitive disorder. Findings to date suggest a reduced risk of Alzheimer’s disease and improved cognitive functioning of postmenopausal women who use 17β-estradiol. With regards to Parkinson’s disease, there is consistent evidence from basic science studies for a neuroprotective effect of 17β-estradiol; however, results of clinical and epidemiological studies are inconclusive at this time, and there is a paucity of research examining the association between HRT and Parkinson’s-related neurocognitive impairment. Even less understood are the effects of HRT on risk for frontotemporal dementia and HIV-associated neurocognitive disorder. Limits to the existing research are discussed, along with proposed future directions for the investigation of HRT and neurodegenerative diseases.


2019 ◽  
Vol 4 (4) ◽  
pp. 607-614
Author(s):  
Jean Abitbol

The purpose of this article is to update the management of the treatment of the female voice at perimenopause and menopause. Voice and hormones—these are 2 words that clash, meet, and harmonize. If we are to solve this inquiry, we shall inevitably have to understand the hormones, their impact, and the scars of time. The endocrine effects on laryngeal structures are numerous: The actions of estrogens and progesterone produce modification of glandular secretions. Low dose of androgens are secreted principally by the adrenal cortex, but they are also secreted by the ovaries. Their effect may increase the low pitch and decease the high pitch of the voice at menopause due to important diminution of estrogens and the privation of progesterone. The menopausal voice syndrome presents clinical signs, which we will describe. I consider menopausal patients to fit into 2 broad types: the “Modigliani” types, rather thin and slender with little adipose tissue, and the “Rubens” types, with a rounded figure with more fat cells. Androgen derivatives are transformed to estrogens in fat cells. Hormonal replacement therapy should be carefully considered in the context of premenopausal symptom severity as alternative medicine. Hippocrates: “Your diet is your first medicine.”


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