Parkinson’s disease, a dopaminergic (DA) degeneration of nigrostriatal neurons of still unknown etiology, affects about 2% of the population over 65 years of age. Recently, it has been proposed that one possible cause of dopaminergic cell death is the overactivation of the brain renin–angiotensin system (RAS), which operates locally and independently from the peripheral system. This system, present in the substantia nigra and striatum, becomes hyperactivated through AT1 receptors, inducing oxidative stress and promoting inflammatory responses, thereby facilitating DA neurodegeneration and rarefaction of the brain microvasculature. In addition, reduced circulating levels of IGF-1, characteristic of aging and neuroinflammation, increase the risk of cerebral microvascular damage and cerebromicrovascular dysfunction. These processes are interconnected and mutually reinforcing. In this context, we evaluated, in early stages of the disease, changes in the microvasculature such as blood–brain barrier damage in a parkinsonian animal model. We propose an integrative therapeutic approach to counteract these alterations: administration of the drug candesartan, which blocks AT1 receptors, together with adenovectors to enhance IGF-1 expression in our animal model.