Intraventricular α-interferon in subacute sclerosing panencephalitis

Cianchetti, Carlo; Marrosu, Maria Giovanna; Muntoni, F.; Fratta, Annalisa; Zuddas, Alessandro

doi:10.1212/wnl.50.1.315

Cited by 11 publications

(4 citation statements)

References 2 publications

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“…This short-term NPY effect could have implications for IFN-· immunotherapy. For example, in conditions where IFN-· is administered intracerebroventricularly or intrathecally [12][13][14][15][16], the NPY short-term effect could be timed to coordinate with the eating schedule of a subject receiving IFN-· therapy. This will maximize the feeding induction properties of NPY, while not influencing hunger at times where it would be inappropriate (during sleeping periods, for example).…”

Section: Discussionmentioning

confidence: 99%

“…The dose of IFN-· used in these experiments was based on an immunotherapeutic dose administered intracerebroventricularly or intrathecally for the treatment of subacute sclerosing panencephalitis [12][13][14][15][16]. A dose of 1 !…”

Section: Intracerebroventricular Microinfusionmentioning

confidence: 99%

“…IFN-· is used in the treatment of solid tumors [4][5][6], leukemia [5], and chronic infections including hepatitis B [4,5,7], C [8][9][10][11] and subacute sclerosing panencephalitis [12][13][14][15][16].…”

Section: Introductionmentioning

confidence: 99%

“…In a clinical setting, IFN-· immunotherapy into the brain involves the repeated intraventricular or intrathecal infusion of IFN-· several times a week [12][13][14][15][16]. Consequently, the IFN-·-induced anorexia could be associated with weight loss and changes in metabolic activities [22,30].…”

Section: Introductionmentioning

confidence: 99%

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Neuropeptide Y Counteracts Interferon-Alpha-Induced Anorexia

Turrin¹,

Flynn²,

Plata‐Salamán³

1999

Neuroimmunomodulation

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Interferon-α (IFN-α) immunotherapy is associated with significant adverse neurological effects, including anorexia, which can be a limiting factor in immunotherapy. Thus, it is important to develop strategies that could ameliorate IFN-α-induced neurological manifestations without significantly affecting its immunomodulating properties. In this study, we tested the hypothesis that an endogenous feeding-enhancing peptide, neuropeptide Y (NPY), could inhibit IFN-α-induced anorexia in rats. The results show that IFN-α induced significant anorexia when administered centrally into the third cerebral ventricle at an immunotherapeutically relevant dose (1,350 IU/rat). Heat-inactivated IFN-α had no effect. NPY (5.0 µg/rat) counteracted the IFN-α-induced anorexia when administered 3 or 10 h following IFN-α, or when it was concomitantly administered with IFN-α. The data suggest that NPY and its agonists could represent a potential novel intervention for IFN-α immunotherapy-associated anorexia.

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