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A lzheimer’s disease (AD) is the most severe neurodegenerative disorder affecting the elderly. The exact pathology of AD remains unclear, but key features include amyloid-β deposition, tau hyperphosphorylation, neuroinflammation, and dysfunctions in mitochondria, metal ions, autophagy, and the cholinergic system. Despite the absence of a definitive treatment for AD, numerous natural products have shown potential in preventing and slowing disease progression. Algae, a rich source of bioactive compounds, offers promising neuroprotective substances for AD management. Fucoxanthin and astaxanthin, carotenoids found in algae, have demonstrated neuroprotective effects through antioxidant and anti-inflammatory properties. These compounds inhibit acetylcholinesterase (AChE), butyrylcholinesterase (BuChE), β-secretase (BACE-1), and monoamine oxidase (MAO), suppress amyloid-β accumulation, prevent apoptosis induced by Aβ1–42 and H2O2, and modulate antioxidant enzymes such as superoxide dismutase (SOD) and catalase (CAT) by inhibiting the ERK pathway. Cellular and animal studies have further highlighted the benefits of fucoxanthin and astaxanthin in AD, showcasing their efficacy in managing the disease through multiple targets.

Neurodegenerative diseases are expected to become the second leading cause of death among the elderly by the 2040s. These diseases are associated with microvascular dysfunction, neurovascular disintegration, defective blood-brain barrier (BBB) function, and vascular factors. AD, the most common form of dementia, is characterized by significant neuron loss and specific histopathological brain changes. It leads to memory loss, behavioral disturbances, personality changes, and cognitive decline. The increasing prevalence of AD due to aging populations is a significant clinical and socioeconomic burden.

AD is categorized into early-onset AD (EOAD), which accounts for 1-5% of cases, and late-onset AD (LOAD), accounting for over 95% of cases. Genetic risk factors include mutations in the amyloid precursor protein (APP), presenilin 1 (PSEN1), and presenilin 2 (PSEN2) genes, which are involved in APP breakdown and amyloid-β generation. LOAD is associated with polymorphisms in the apolipoprotein E (APOE) gene, especially the ε4 allele, and alterations in the triggering receptor expressed on myeloid cells 2 (TREM2) gene. Non-genetic risk factors include cerebrovascular disease, hypertension, diabetes, dyslipidemia, smoking, traumatic brain injury, stress, depression, and inadequate sleep.

AD pathology involves abnormal extracellular amyloid-β plaques and intracellular hyperphosphorylated tau neurofibrillary tangles. These protein abnormalities lead to complex and multifactorial neurodegeneration. Approved pharmacological treatments for AD focus on symptomatic management, but marine algae have been recognized as a potential source of pharmaceutical and nutraceutical compounds. Algae, including Chlorophyceae (green algae), Phaeophyceae (brown algae), and Rhodophyceae (red algae), produce secondary and primary metabolites with significant biological activities.

Carotenoids, due to their polyisoprenoid structure with conjugated double bonds, exhibit various pharmacological activities, including antioxidant and anti-inflammatory effects. These lipid-soluble molecules protect the brain from oxidative stress, neuroinflammation, and mitochondrial dysfunction, common in neurodegenerative diseases. Fucoxanthin and astaxanthin, two such carotenoids, offer therapeutic potential for AD. This review explores the pathophysiology of AD and the therapeutic benefits of fucoxanthin and astaxanthin, discussing their pharmacokinetic properties and delivery systems to the central nervous system (CNS).

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