Parkinson's disease (PD) is the second most common neurodegenerative disease, affecting around 1% of adults older than 60 years. Patients with PD clinically manifested by symptoms of motor movement disorder such as rigidity, resting tremor and bradykinesia. Furthermore, PD has an association with non-motor symptoms such as gastrointestinal dysfunction, olfactory deficits, depression, cognitive decline, disruption of sleep wake cycle and anxiety, and Non-motor symptoms clearly precede the onset of motor symptoms. PD is characterized by the progressive neurodegeneration of dopamine in the substantia nigra pars compacta (SNpc), and the loss of those neurons is mainly associated with the motor symptoms. Because until today there is no disease modifying treatment for PD, its essential to look for new potential medications that can modify disease pathology, Telmisartan is one such medication that has shown potential experimentally in reducing neuroinflammation and it will be investigated in the study for its possible value in reducing indicators of nigrostriatal damage as seen in PD. Aim: The main purpose of this study is to invvestigate the effects of telmisartan on the lipopolysaccharide (LPS) rat model of PD. This will be done by comparing LPS-lesioned rats in the absence and presence of telmisartan. LPS which is a bacterial toxin most commonly delivered into the striatum and substantia nigra (SN), making it useful for studying the precise effects of inflammation on dopamine neurons within the SN and their neuronal projection to the striatum. This LPS model displaying selective neurodegeneration of dopamine within the SN and their neuronal projection to the striatum. Method: Thirty male wistar rats weighing between (200-220) g, were randomized and divided into 5 different groups of 6 rats per group. Group A considered the control group, group B was given telmisartan alone, group C LPS alone, group D LPS lesioned rats were treated with oral telmisartan (3 days before surgery and continued until apomorphine test). finally, group E was subjected to LPS + telmisartan orally for 7 days (from day 7 to day 14) after surgery. Result: Fourteen days post intranigral adminstration of LPS, and following an apomorphine challenge, LPS lesioned rats receiving telmisartan either before or after surgery significantly reduced number of complete rotations compared to LPS only group. compatible with these findings, concentrations of the striatal tissue dopamine were significantly higher in groups D and E (either 3 days before LPS lesioning or 7 days after LPS lesioning) versus group C (LPS only group). Also, telmisartan reduced the levels of TNF- ? in groups D and E in comparison with group C. The brain-derived neurotrophic factor (BDNF) levels in the striatum were reduced in both telmisartan with LPS groups (3 days before LPS lesioning or 7 days after LPS lesioning) in comparison to LPS only treated rats. Conclusion: This study proved that telmisartan has a neuroprotective properties which can protect dopaminergic neurons and has the ability to alleviate and delay the pathophysiological process of PD and to reduce the inflammatory response.