Failure of Amantadine Hydrochloride to Alter Immune Responses in the Experimental Allergic Encephalomyelitis Model of Neuroautoimmune Disease

Abstract

Amantadine hydrochloride has been reported efficacious in the symptomatic management of patients with multiple sclerosis (MS). To characterize further the potential effects of amantadine in MS, we studied the drug's effect on immunological parameters in the experimental allergic encephalomyelitis (EAE) model. Nine Lewis rats were used; 3 served as controls and 6 were EAE-induced. Three of the EAE-induced rats received amantadine (AMT) (0.3 g/kg/day) at the onset of EAE symptoms. Sera were collected post-AMT treatment and assayed for antimyelin basic protein antibody (anti-MBP) and 2′3′-cyclic nucleotide 3′-phosphohydrolase activity (CNP). The mean differences in the immunological parameters between treated and nontreated EAE-induced groups were not significant. These findings fail to demonstrate a spscific effect of amantadine on immunologic responses tested in the EAE model, and do not support the notion that the effects of amantadine in MS are linked to basic alterations in immune responses.

Key Words:

• amantadine hydrochloride
• experimental allergic encephalomyelitis
• multiple sclerosis
• neuro-autoimmune disease
• 2′3′-cyclic nucleotide 3′-phosphohydrolase activity
• anti-myelin basic protein antibody
• neuroimmunomodulalion

Additional information

Notes on contributors

Reuven Sandyk

Joyce Laing works in the Department of Child and Family Psychiatry, Playfield House, Cupar, Fife, and is a Consultant Art Therapist to Psychiatric Hospitals and Prisons and Chairwoman of the Scottish Society of Art and Psychology.