## 3 AD and PD and Bioactive Rosemary Compounds with Health-Promoting Effects
### Parkinson's Disease  
Parkinson's disease (PD), commonly known as \"Shaking Palsy\", is the second most common chronic neurodegenerative disorder (ND) affecting people, especially those at advanced ages, and is mainly attributed to the absence of dopaminergic (DAergic) neurons in the substantia nigra (SN). The SN is a part of the brain responsible for the movement of the human body, where DArgic neurons control the production of the neurotransmitter dopamine (DA) in the striatum. DA is responsible for regulating some functions in the human body, including the functioning of the hormonal and cardiovascular systems [9; 28; 29]. In 2019, almost 8.5 million people had PD according to the World Health Organization (WHO) [22; 30]. The neurons implicated in PD are more vulnerable to oxidative stress and inflammation due to their elevated levels of lipids and fatty acids (FAs), which lead to lipid peroxidation. DA is also vulnerable to auto-oxidation, resulting in high levels of catecholamine quinones (DAQs) and H\({}_{2}\)O\({}_{2}\) (an ROS), thus leading to oxidative damage [1; 22; 28; 31; 32; 33]. There are various factors involved in the genesis of PD. An enzyme known as tyrosine hydroxylase (TH) facilitates the initial synthesis of the hormone DA within the neurons by catalyzing the conversion of L-tyrosine to L-dopa. L-dopa serves as a progenitor to DA, and its deficiency might lead to low DA levels and PD [10; 34; 35; 36; 37]. Concurrently, additional factors able to trigger the loss of DA are Lewy bodies (LBs), a result of \(\alpha\)-synuclein (\(\alpha\)-syn) aggregation in dopaminergic neurons, and ubiquitits, which are complement and structural cytoplasmic proteins [23]. \(\alpha\)-syn is a protein located mainly in the central nervous system (CNS). The main functions of \(\alpha\)-syn involve regulation of memory, recognition, neurotransmitter release, presynaptic vesicle trafficking, and immunomoddation. Aggregation of this protein may be linked to mitochondrial dysfunction and oxidative stress [19; 23; 35; 38; 39]. Mitochondria are the principal organelles that excessively generate ROS, which can impair mitochondrial constituents like proteins or lipids, and finally lead to mitochondrial dysfunction and the degeneration of mitochondrial components [22; 40]. Glutathione (GSH) is also vital as a thiol tripeptide that functions as an antioxidant against ROS. The symptoms of PD may vary from one individual to another, and can severely affect the patients' lives. The most common symptoms are motor ones, including bradykinesia, lack of postural stability, a resting tremble, and stiffness, but also non-motor symptoms like depression, dementia, sleep disorders, sensory symptoms, and lack of writing and talking abilities [1; 10; 22; 23; 31; 32; 35; 38; 39]. The current medications used to mitigate PD symptoms are synthetic products that have prominent side effects and are relatively unaffordable [42]. The accepted pharmacotherapies for PD include levodopa (L-dopa), catechol-o-methyl transferase inhibitors (COMT-Is), and monoamine oxidase inhibitors (MAO-Is) [39; 42; 43]. L-dopa, specifically, is effective for treating the motor manifestationsof PD with fewer side effects; however, nausea or postural hypotension are possible, while extended administration may result in dangerous symptoms like stroke or dementia [44], as well as dyskinesia [41; 45]. L-dopa, when administered to patients, crosses the blood-brain barrier (BBB) and transforms into DA in the brain, thus preventing the symptoms of PD [41]. With an emphasis on keeping DA levels high, MAO inhibitors like monoamine oxidase type B inhibitors (MAO-BIs) may inhibit DA and levodopa collapse in the brain and alleviate depression in the initial stages of PD [41; 44]. Also, COMT inhibitors are of great interest as they function as enzymes that aid the transportation of L-dopa to the brain, where it undergoes conversion into DA or increases synaptic DA levels.