Antidepressant Effects of Probucol on Early-Symptomatic YAC128 Transgenic Mice for Huntington's Disease

Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder caused by a trinucleotide expansion in the HD gene, resulting in an extended polyglutamine tract in the protein huntingtin. HD is traditionally viewed as a movement disorder, but cognitive and neuropsychiatric symptom...

Ausführliche Beschreibung

Bibliographische Detailangaben
Veröffentlicht in:Neural plasticity. - 1998. - 2018(2018) vom: 10., Seite 4056383
1. Verfasser: de Paula Nascimento-Castro, Cristine (VerfasserIn)
Weitere Verfasser: Wink, Ana Claudia, da Fônseca, Victor Silva, Bianco, Claudia Daniele, Winkelmann-Duarte, Elisa C, Farina, Marcelo, Rodrigues, Ana Lúcia S, Gil-Mohapel, Joana, de Bem, Andreza Fabro, Brocardo, Patricia S
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2018
Zugriff auf das übergeordnete Werk:Neural plasticity
Schlagworte:Journal Article Research Support, Non-U.S. Gov't Antidepressive Agents Antioxidants Dcx protein, mouse Doublecortin Protein Cholesterol 97C5T2UQ7J Probucol P3CTH044XJ
LEADER 01000naa a22002652 4500
001 NLM288238451
003 DE-627
005 20231225055825.0
007 cr uuu---uuuuu
008 231225s2018 xx |||||o 00| ||eng c
024 7 |a 10.1155/2018/4056383  |2 doi 
028 5 2 |a pubmed24n0960.xml 
035 |a (DE-627)NLM288238451 
035 |a (NLM)30186318 
040 |a DE-627  |b ger  |c DE-627  |e rakwb 
041 |a eng 
100 1 |a de Paula Nascimento-Castro, Cristine  |e verfasserin  |4 aut 
245 1 0 |a Antidepressant Effects of Probucol on Early-Symptomatic YAC128 Transgenic Mice for Huntington's Disease 
264 1 |c 2018 
336 |a Text  |b txt  |2 rdacontent 
337 |a ƒaComputermedien  |b c  |2 rdamedia 
338 |a ƒa Online-Ressource  |b cr  |2 rdacarrier 
500 |a Date Completed 27.11.2018 
500 |a Date Revised 04.12.2021 
500 |a published: Electronic-eCollection 
500 |a Citation Status MEDLINE 
520 |a Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder caused by a trinucleotide expansion in the HD gene, resulting in an extended polyglutamine tract in the protein huntingtin. HD is traditionally viewed as a movement disorder, but cognitive and neuropsychiatric symptoms also contribute to the clinical presentation. Depression is one of the most common psychiatric disturbances in HD, present even before manifestation of motor symptoms. Diagnosis and treatment of depression in HD-affected individuals are essential aspects of clinical management in this population, especially owing to the high risk of suicide. This study investigated whether chronic administration of the antioxidant probucol improved motor and affective symptoms as well as hippocampal neurogenic function in the YAC128 transgenic mouse model of HD during the early- to mild-symptomatic stages of disease progression. The motor performance and affective symptoms were monitored using well-validated behavioral tests in YAC128 mice and age-matched wild-type littermates at 2, 4, and 6 months of age, after 1, 3, or 5 months of treatment with probucol (30 mg/kg/day via water supplementation, starting on postnatal day 30). Endogenous markers were used to assess the effect of probucol on cell proliferation (Ki-67 and proliferation cell nuclear antigen (PCNA)) and neuronal differentiation (doublecortin (DCX)) in the hippocampal dentate gyrus (DG). Chronic treatment with probucol reduced the occurrence of depressive-like behaviors in early- and mild-symptomatic YAC128 mice. Functional improvements were not accompanied by increased progenitor cell proliferation and neuronal differentiation. Our findings provide evidence that administration of probucol may be of clinical benefit in the management of early- to mild-symptomatic HD 
650 4 |a Journal Article 
650 4 |a Research Support, Non-U.S. Gov't 
650 7 |a Antidepressive Agents  |2 NLM 
650 7 |a Antioxidants  |2 NLM 
650 7 |a Dcx protein, mouse  |2 NLM 
650 7 |a Doublecortin Protein  |2 NLM 
650 7 |a Cholesterol  |2 NLM 
650 7 |a 97C5T2UQ7J  |2 NLM 
650 7 |a Probucol  |2 NLM 
650 7 |a P3CTH044XJ  |2 NLM 
700 1 |a Wink, Ana Claudia  |e verfasserin  |4 aut 
700 1 |a da Fônseca, Victor Silva  |e verfasserin  |4 aut 
700 1 |a Bianco, Claudia Daniele  |e verfasserin  |4 aut 
700 1 |a Winkelmann-Duarte, Elisa C  |e verfasserin  |4 aut 
700 1 |a Farina, Marcelo  |e verfasserin  |4 aut 
700 1 |a Rodrigues, Ana Lúcia S  |e verfasserin  |4 aut 
700 1 |a Gil-Mohapel, Joana  |e verfasserin  |4 aut 
700 1 |a de Bem, Andreza Fabro  |e verfasserin  |4 aut 
700 1 |a Brocardo, Patricia S  |e verfasserin  |4 aut 
773 0 8 |i Enthalten in  |t Neural plasticity  |d 1998  |g 2018(2018) vom: 10., Seite 4056383  |w (DE-627)NLM098558390  |x 1687-5443  |7 nnns 
773 1 8 |g volume:2018  |g year:2018  |g day:10  |g pages:4056383 
856 4 0 |u http://dx.doi.org/10.1155/2018/4056383  |3 Volltext 
912 |a GBV_USEFLAG_A 
912 |a SYSFLAG_A 
912 |a GBV_NLM 
912 |a GBV_ILN_21 
912 |a GBV_ILN_350 
951 |a AR 
952 |d 2018  |j 2018  |b 10  |h 4056383