Since ApoD is a small protein implicated in many pathologies, and its mechanistic mode of action is largely unknown, its therapeutic potential has yet to be fully understood. For now, since it positively affects oxidative stress, downregulates inflammation, and also has relatively positive effects on the metabolic syndrome in some tissues, its potential as a therapeutic protein can be considered high, and its effects are worth exploring [13].

Parkinson's disease is connected to a pathological events related to inflammation as well as oxidative stress, which are thought to contribute to dopaminergic neurodegeneration through a neurotoxic process mediated by free radicals [14].

Apolipoprotein D changes AA hydroperoxides into lipid hydroxides, which inhibits lipid peroxidation chain reactions and modifies the inflammatory pathways in PD [10].

This study showed that individuals with PD had considerably greater blood levels of Apo D than the controls. This finding is consistent with that obtained by Waldner and his group [4].

No difference in serum level of Apo D was observed in our study in PD patients among the genders which is in agreement with Waldner and his colleagues in their study [4]. Previous studies explained that Apo D level is increased in response to neurodegeneration and oxidative stress [15], and this has no relation to the patients’ gender [16].

We showed in our study that there was no statistically significant difference between TD, and BRD phenotypes in terms of age and duration of disease, which is consistent with previous study [16].

According to other researches, PD patients with TD who still experience it after several years progress more slowly than those who suffer from other motor symptoms [11, 17, 18]. Also patients with BRD experience significantly greater subjective motor and occupational impairment than people with TD [19].

When comparing the serum level of Apo D and clinical types of the patient, there was a statistically significant difference with higher mean of Apo D serum level among BRD phenotype. This finding agrees with Selikhova and his group, who noted that PD cases with bradykinesia and rigidity predominant have a more pathological burden [20]. Autopsy results from neuroimaging studies have revealed higher levels of dopaminergic denervation and grey matter atrophy [21, 22], with resultant increased Apo D in response to neurodegeneration [15].

By applying the immunohistochemistry technique in a previous research, it has been shown a significant rise in the Apo D positive cells' number, predominantly glial cells, in the cortex of the aging human. Apo D protects against age-related oxidative stress caused by rising ROS levels via its antioxidant and anti-inflammatory action [5]. However, in this study, there was no statistically significant correlation between the serum level of Apo D and the patients' age in contrast to Waldner and his colleagues, who demonstrated a significant association in cases older than 65 years old [4]. This contradiction could be attributed to the difference in age group, as the mean age of their patients was 72.84 ± 7.07 while the mean age of our studied group was 53. 6 ± 12.9.

Finally, our results showed a significant positive association between Apo D serum levels and disease intensity as evaluated by the UPDRS, which is consistent with the findings of Waldner and his group [4].

These results are explained by Apo D growing involvement in shielding cells against astrogliosis, leading to worsening PD motor symptoms. When out of control, reactive astrocytes can be an obstacle because they are necessary to replace the lost dopaminergic neurons and prevent further damage from spreading. As a result, astrogliosis is a “two-edged sword”. Apo D has been hypothesized to play a function in keeping the glial response to many ROS/RNS and inflammatory mediators within set limits [5].