# Seareed Exhibits Therapeutic Properties against Chronic Diseases: An Overview
## 6 Pharmacological Properties of Seaweed to Overcome Chronic Disease
### Neurodegenerative Disease
One of the factors causing misfolded proteins that is associated with neurodegenerative diseases is increased endoplasmic reticulum (ER)  
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stress. Ethanol extract from _Undaria pinnatifida_ was reported to decrease endoplasmic reticulum (ER) voltage through the Akt/mTOR signaling pathway [133]. Fucoxanthin extract of _Sargassum lorneri_ showed neurodegenerative effects by decreasing H2O2-induced neurotoxicity via upregulating of the PI3K/Akt cascade and inhibition of the ERK pathway [107]. Bisindole alkaloids, namely racemocin A and racemocin B from _Caulerpa racemose_, reduced the A\(\beta\)25-35-induced SH-SYSY cell (neuroblast from neural tissue) damage by increasing cell viability of 5.5% and 14.6% for racemocin A and racemocin B, respectively [114]. Fucoxanthin may rescue cerebral ischemic/reperfusion injury from nerve inflammation and oxidative stress by promoting the Nrf/HO-1 signaling pathway in rats [21]. Reducing Ca2+-mediated neurotoxicity could protect rats with cerebral ischemic/reperfusion injury from nerve inflammation and oxidative stress [136]. [PERSON]'s disease is a type of dementia that causes a global, progressive, and irreversible deterioration of various cognitive functions (memory, attention, concentration, language, and thinking, among others) [144]. The main cause of [PERSON]'s disease is the dysregulation of \(\beta\)-amyloid (A\(\beta\)) levels, which induces neuronal death via multiple mechanisms, including oxidative stress, excitotoxicity, apoptosis, and inflammation [145]. According to [PERSON] et al. [135], _Islige foliacea_ may decrease A\(\beta\) accumulation, thus inhibiting AChE and BACE1 [134], and suppress memory deficits by enhancing the BDNF-TrkB-ERK signaling pathway in the hippocampus. Butanol extracts from _Ecklonia cava_ have anti-A\(\beta\) effects on A\(\beta\)-related pathogenesis, including amyloidogenic processing, A\(\beta\) oligomerization, A\(\beta\) fibrillization, and A\(\beta\)-induced neuronal death [137]. By downregulating the ERK, p38 MAPK, and JNK pathways, compounds isolated from _Islige okamurae_ reduced A\(\beta\)25-35-induced phosphorylation both in vitro and in vivo [39]. Phenolic compounds from _Gracilaria beckeri_, _Ecklonia maxima_, _Gelidium pristoides_, and _Ultra rigida_, such as phloroglucinol, catechin, and epicatechin 3-glucoside, significantly reduced anti-acetylcholinesteraseterase and butyrylcholinesteraseterase activities [140]. [PERSON]'s disease is a prevalent neurological disease affecting the movement of the elderly. It is characterized by the formation of Lewy bodies, the death of dopaminergic neurons in the substantia nigra pars compacta (SNP), and dopamine depletion (DA) [116, 146]. During aging, the concentration of iron in the brain can change, resulting in metabolic stress [147, 148]. The neuroprotective activity of _Bifurcaria bifurcata_ fractions suggested that two major diterpenes (eleganolone and eleganonal) have potential for [PERSON]'s disease management because of their iron-reducing activities [116]. [PERSON] et al. [149] reported that among the three macroalgae tested, _Sacorhiza polyschides_ exhibited the highest potential as a therapeutic agent against AD-induced toxicity, exhibiting anti-apoptotic effects associated with mitochondrial protection and caspase-3 inhibition in a model of [PERSON]'s disease. Two extracts, _Undaria pinnatifida_ and fucoxanthin, showed moderate inhibition and were inactive against _h_MAO-A and _h_MAO-B [135]. These results suggest that fucoxanthin may be beneficial for [PERSON]'s disease due to its ability as a potent dopamine D3/D4 agonist agent. An in vivo study reported that rats fed sulfated agaran exhibited great neuroprotection due to its ability to reduce oxidative stress, and showed recovery of behavioral activity and improved weight gain [141]. Based on previous research, extracts of phlorotannins and their derivatives from brown seaweed demonstrate neuroprotective activity.