Parkinson's disease patients with bilateral subthalamic deep brain stimulation gain weight

Macia, F.; Perlemoine, Caroline; Coman, Irène; Guehl, Dominique; Burbaud, Pierre; Cuny, Emmanuel; Gin, H.; Rigalleau, Vincent; Tison, François

doi:10.1002/mds.10630

Cited by 112 publications

(136 citation statements)

References 27 publications

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“…Although the cause is still debated, gastrointestinal dysfunction had been suggested due to the often-occurring degeneration of the enteric nervous system during disease progression (30). It is plausible, however, that the diminished DA innervation to the CPu is the cause for the weight loss, because patients with subthalamic deep-brain stimulation gain weight after onset of treatment (31,32). To determine whether the degeneration of the nigrostriatal system in En HT mice is accompanied by lower weight, we recorded the body weight of the mutants and their En2Ϫ͞Ϫ littermate controls over their entire lifespan (Fig.…”

Section: Molecular Changes In Basal Ganglia Of En Ht Micementioning

confidence: 99%

Slow progressive degeneration of nigral dopaminergic neurons in postnatal Engrailed mutant mice

Sgadò

Albèri

Gherbassi

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

133

132

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The homeobox transcription factors Engrailed-1 and Engrailed-2 are required for the survival of mesencephalic dopaminergic neurons in a cell-autonomous and gene-dose-dependent manner. Because of this requirement, the cells die by apoptosis when all four alleles of the Engrailed genes are genetically ablated (En1؊͞؊; En2؊͞؊). In the present study, we show that viable and fertile mice, heterozygous null for Engrailed-1 and homozygous null for Engrailed-2 (En1؉͞؊;En2؊͞؊), have an adult phenotype that resembles key pathological features of Parkinson's disease. Specifically, postnatal mutant mice exhibit a progressive degeneration of dopaminergic neurons in the substantia nigra during the first 3 mo of their lives, leading to diminished storage and release of dopamine in the caudate putamen, motor deficits similar to akinesia and bradykinesia, and a lower body weight. This genetic model may provide access to the molecular etiology for Parkinson's disease and could assist in the development of novel treatments for this neurodegenerative disorder.dopamine ͉ midbrain ͉ mouse mutant ͉ neurodegenerative disease ͉ substantia nigra M esencephalic dopaminergic (mesDA) neurons are the main source of dopamine in the mammalian central nervous system (1). They are located in three distinct nuclei, the substantia nigra pars compacta (SN), the ventral tegmentum (VTA), and the retrorubral field (RRF). Their main innervation targets are the basal ganglia, where they play a major role in controlling emotion, motivation, and motor behavior (2, 3), recognized by their involvement in schizophrenia, addiction, and most prominently in Parkinson's disease (PD; ref. 4). PD is a multisystemic degenerative disorder of the central and peripheral nervous systems. Its hallmark is the progressive degeneration of DA neurons in the SN. The clinical symptoms are resting tremor; muscular rigidity; postural instability; hyposomia; a positive response to the application of L-3,4-dihydroxyphenylalanine (L-DOPA); and the presence of cytoplasmatic inclusions (Lewy bodies) in postmortem brains (5). Additionally, PD patients are often characterized by weight loss starting before diagnosis and continuing with disease progression (6, 7).The homeodomain transcription factors Engrailed-1 and -2 (En1 and En2) are expressed by all mesDA neurons soon after differentiation and then continuously into adulthood. They are cell-autonomously and in a gene-dose-dependent manner required for the survival of this neuronal population, leading to the complete loss of the cells in mutant mice homozygous null for both genes (En1Ϫ͞Ϫ;En2Ϫ͞Ϫ; refs. 8 and 9). In their function as survival factors for mesDA neurons, the two genes are redundant and can compensate for each other (9, 10). The single-null mutants for either En1 (En1Ϫ͞Ϫ) or En2 (En2Ϫ͞Ϫ) show no significant alterations in the organization of the mesDA system at birth, but the mice with genotypes intermediate to the single and double mutants are distinctively different from each other. Whereas En1Ϫ͞Ϫ;En2ϩ͞Ϫ mice die at po...

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Section: Molecular Changes In Basal Ganglia Of En Ht Micementioning

confidence: 99%

Slow progressive degeneration of nigral dopaminergic neurons in postnatal Engrailed mutant mice

Sgadò

Albèri

Gherbassi

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

133

132

View full text Add to dashboard Cite

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“…Despite extensive research, there is still no unified concept explaining the mechanism of DBS-STN, namely the non-motor effects. Body weight variation has been reported in many studies as a non-motor secondary effect of DBS-STN [7][8][9][10]. Studies have shown that weight loss in patients with PD before surgery is a continuous and progressive process that starts years before a formal diagnosis is made, and that surgery modifies this state [11][12][13][14].…”

Section: Deep Brain Stimulation Of Subthalamic Nucleus (Dbs-stn) Offersmentioning

confidence: 99%

Evaluation of Metabolic State in Striatal Rat Model of Parkinson’s Disease: before and after Deep Brain Stimulation

Guimarães¹,

Moura²,

Silva³

et al. 2013

J Obes Weight Loss Ther

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“…One of the most common chronic side-effects of DBS is weight gain (Moro et al, 1999;Barichella et al, 2003;Krack et al, 2003;Macia et al, 2004;Perlemoine et al, 2005;Kleiner-Fisman et al, 2006;Montaurier et al, 2007;Bannier et al, 2009;Sauleau et al, 2009;Walker et al, 2009;Strowd et al, 2010;Locke et al, 2011;Rieu et al, 2011). Typically, weight gain is maximal in the first year after surgery (Barichella et al, 2003;Macia et al, 2004).…”

Section: Chronic Issuesmentioning

confidence: 99%

Postoperative management of deep brain stimulation in Parkinson’s disease

Castrioto

Volkmann

Krack

2013

Handbook of Clinical Neurology

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Parkinson's disease patients with bilateral subthalamic deep brain stimulation gain weight

Cited by 112 publications

References 27 publications

Slow progressive degeneration of nigral dopaminergic neurons in postnatal Engrailed mutant mice

Slow progressive degeneration of nigral dopaminergic neurons in postnatal Engrailed mutant mice

Evaluation of Metabolic State in Striatal Rat Model of Parkinson’s Disease: before and after Deep Brain Stimulation

Postoperative management of deep brain stimulation in Parkinson’s disease

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