## 3 AD and PD and Bioactive Rosemary Compounds with Health-Promoting Effects
### Alzheimer's Disease (AD)  
Alzheimer's disease (AD) is characterized as a divergent neurological impairment, and is currently thought to stem from a variety of different causes and influences. AD's target group is primarily those aged 65 and over [46]. The disease's pathophysiological features, such as amyloid plaque deposits, neurofibrillary tangles, acetylcholine deficiency, lost neuronal connections, hippocampal shrinkage, and others, have been thoroughly investigated and identified in the brains of afflicted patients [47]. The most prominent explanations for the causes of AD are the cholinergic hypothesis, amyloid cascade hypothesis, mitochondrial cascade hypothesis, and oxidative stress theory [48]. It is posited that the pivotal factor in provoking AD is oxidative stress. As a result of its heightened oxygen expenditure, the cerebral region is explicitly susceptible to oxidative stress. Whether this phenomenon is a causative agent or manifests as a direct consequence of AD remains a subject of ongoing  
Figure 1: Connections between neuroinflammation, systemic inflammation, and PD occurrence in the cerebrum. Factors like TNF-\(\alpha\) and IL-6, as well as blood cells including eosinophils, neutrophils, lymphocytes, and monocytes, are able to induce many proinflammatory cytokines that can initiate the degeneration of neurons via a-syn in the process of ongoing neuroinflammation, which induces the progression of PD. investigation [49; 50]. It is intimately connected with the existence of \(\beta\)-amyloid oligomers and specifically pertains to the incapacity to eliminate the neuro-disrupting compound known as 4-hydroxynonenal (HNE) which is significantly associated with the increased probability of disease development and augmentation [51]. Empirical work has indicated that apolipoprotein E (APOE) has the lion's share in upholding body homeostasis by regulating the oxidative damage status [52]. The inheritance of the apolipoprotein E4 (APOE4) allele is implicated in the progression of AD. This mutated protein is ineffective at HNE elimination [53]. Furthermore, APOE4 may catalyze HNE formation and facilitate binding to nerve proteins [54]. The presence of APOE4 is causatively linked to neuronal dysfunction, potentially due to the absence of cysteine (Cys) residues, which are pivotal in averting lipid peroxidation [55; 56]. Hence, possessing the APOE4 allele is closely correlated with elevated peroxid oxidized lipid levels [52]. APOE4 also can trigger oxidative stress through its interaction with mutated manganese superoxide dismutase (MnSOD). Notably, individuals carrying this gene exhibit dysfunctional glucose metabolism at a young age, preceding the manifestation of the disorder's symptoms [54]. The mitochondrial aging hypothesis arose because \(\beta\)-amyloid (A\(\beta\)) affects the activity of mitochondrial enzymes [57; 58]. In light of this fact, scientists have investigated the functioning of the mitochondrial complexes (I, II, III, and IV). The most conspicuous alterations were detected in complexes I and II. Inhibition of complex I correlated with diminished tau protein production and A\(\beta\) production. Furthermore, complex I played a crucial role in the nexus between oxidative stress and AD [58; 59]. As the body ages, reactive ROS accumulate, thereby fostering the development of oxidative stress. Moreover, the mitochondria house indispensable enzymes responsible for combating ROS. Specifically, mitochondrial dysfunction can be conspicuously observed in the cerebral regions associated with the genesis of AD [59; 60]. Scientists embarked on an inquiry to elucidate the correlation between NADPH oxidase (NOX), responsible for ROS generation, and AD [61]. The NOX protein causes lipid peroxidation and cell death in cancerous cells, among its various roles. Moreover, it mediates ROS generation by upregulating the extracellular signal-regulated kinase (ERK) mechanism. Upon scrutinizing the cerebrum of AD-afflicted mice, an elevated level of NOX-responsive interposed compounds was discerned.