Parkinson's disease (PD) is a common condition that, in the majority of cases, is idiopathic in origin. The loss of central dopaminergic pathways is well-known and in this paper a theory is presented that this is brought about by an autoimmune process. The lack of any HLA association or familial clumping for the disease does not exclude such a theory, as a common etiological agent may exist that we do not yet recognize, e.g., infection, or drugs. Several autoantibodies and disturbances in T-cell function have been found in PD. The theory proposes that the production of autoantibodies and T-cell activation are important in the pathogenesis of idiopathic PD by an action on the substance P striatonigral pathway and its input to the dopaminergic nigrostriatal pathway. The autoimmune destruction of the substance P input leads to a secondary loss of the dopaminergic system and hence PD.