One of the important causes of dementia is AD where dysfunctions of the medial temporal lobe (MTL) and the hippocampus of the brain occur. Patients with AD initially face reduced episodic memory, which leads to gradually affected extensive cognitive dysfunctions like apraxia, amnesia, and visuospatial deficits (Eramudugolla et al., 2017). The pathogenesis of AD is characterized by hyperphosphorylated tau protein (p-tau) in neurofibrillary tangles and the aggregation of the amyloid-β (Aβ) protein in senile plaques in the brain (Moghadas et al., 2020). The abnormal clusters of protein fragments formed between nerve cells are plaques, while the tangles are described as dead nerve cells. The clumping of these small protein fragments is responsible for forming plaques that hamper cell communication by disrupting cell signaling at synapses. However, the tangles are used to destroy a protein from a vital cell transport system. Thus, disease disrupts neuron-related processes and functional networks with their activities, such as communication, metabolism, and repair systems. The sticky beta-amyloid that surrounds nerve cells is present in the lipid bilayer membrane. Another cause of AD progression is an accumulation of Th1 cells and M1 microglial cells in the brain due to the peripheral deposition of phenylalanine and isoleucine by alteration of the gut microbiome (Wang X. et al., 2019). The disease is typically considered a brain disorder that diminishes a large number of neurons in the brain region responsible for learning and memory, i.e., the entorhinal cortex, hippocampus region, and cerebral cortex region involved in speech and social behavior. Therefore, it diminishes memory, thinking skill abilities, and behavioral manifestations, finally leading to dementia with impairment of memory and cognitive judgments.

ALS is a multisystem neurodegenerative fatal disorder in which loss of muscular control occurs due to progressive degeneration of nerve cells in the brain and in the spinal cord. ALS could be due to the involvement of genetic inheritance (familial: fALS) and environmental factors (sporadic: sALS) as well as aging‐related dysfunctions that affect the motor system due to the loss of both upper and lower motoneurons in the motor cortex of the brainstem and anterior horn of the spinal cord. ALS disease is also termed Lou Gehrig’s disease based on the name of a famous baseball player who was diagnosed initially whereas the term “amyotrophic lateral sclerosis” was given by the French neurologist Jean‐Martin Charcot (Masrori and Van Damme, 2020). The hallmarks of ALS include weakness, stiffness, dysarthria, dysphagia, dysphonia, and hyperreflexia. Muscle weakness first starts in the distal muscles and later in the proximal muscles, and wasting occurs. ALS is mainly spread by Mendelian inheritance-associated autosomal dominant gene mutation of Cu/Zn superoxide dismutase (SOD1) and TAR-DNA binding protein 43 (TDP-43) (Grad et al., 2017).

FA is an autosomal recessive degenerative disorder caused by damage to the cerebellum, spinal cord, and peripheral or other nerves or defects or mutations in the FXN gene. The FXN gene holds the genetic code for a mitochondrial protein, called frataxin, i.e., a highly conserved protein, and balanced cellular iron homeostasis (Schmucker and Puccio, 2010). This type of gene mutation is responsible for guanine–adenine–adenine (GAA) trinucleotide repeats in both alleles of FXN genes (Campuzano et al., 1996). The repeated expansion of gene expression reduces the transcription of the gene. This could result in diminished energy production within neurons and cardiac cells. Thus, the result causes poor muscle control and clumsy voluntary movements. Two defective copies of the gene obtained from each parent increase the risk of disease to their offspring. FA is thought to be acquired, degenerative, or hereditary. The term “Friedreich ataxia” was first described by Nikolaus Friedreich and is characterized by motor coordination because of dysfunction of the cerebellum and its connections (Campuzano et al., 1996). The symptoms that may arise are fatigue, nystagmus (involuntary eye movements), hearing loss, dysarthria (slurred speech), cardiomyopathy (heart enlargement), heart failure (CHF), diabetes, difficulty in walking, and sometimes deformities in feet like high arches and curvature of the spine (scoliosis).

Abnormal protein deposits in brain tissues are called Lewy bodies, which result in the decay of brain tissues due to the excess accumulation of abnormal proteins; this condition is called LBD. The disease arises in particular brain regions involved in thinking, learning, memory, and movement. The disease results in dementia; psychiatric symptoms such as visual hallucinations, changes in attention, and alertness; and motor symptoms such as rigid muscles, slow movement, walking difficulty, and tremors.

PD is the second most common neurocognitive and chronic neurodegenerative disorder affecting the nervous system and body parts controlled by the nerves of the nigrostriatal pathway; thus, patients with PD develop both motor and nonmotor features and symptoms (Deal et al., 2019). Dr. James Parkinson, an English physician, initially defined paralysis agitans or shaking palsy in 1817, and the pattern is known as PD (Schnabel, 2010). There are various mutations related to PD, i.e., α-synuclein, LRRK2, PINK1, Parkin, DJ-1, VPS35, GBA1, and the loss of the dopaminergic neuron potential (Zeng et al., 2018). The key pathogenic mechanisms of this disease are mainly oxidative stress and the loss of dopaminergic neurons. This dopaminergic degeneration mainly occurs in the substantia nigra part of the brain since nerve cells, mainly in the substantia nigra region, produce dopamine. Dopamine is a chemical that acts as a neurotransmitter that coordinates body movements. This disease results in uncontrollable movements such as shaking, stiffness, and difficulty balancing and coordinating due to the loss of dopamine neurotransmitters, which are responsible for movement (Deal et al., 2019). In PD, symptoms usually begin gradually and worsen over time. It may also cause mental and behavioral changes, disturbances in sleeping patterns, depression, memory difficulties, and fatigue. As the disease progresses, it becomes more serious, and muscle rigidity and tremors grow due to the slowness of voluntary movement and postural instability.

It is a lethal autosomal dominant mutation that causes HD, a neurodegenerative illness of the central nervous system. HD is an inherited disease that progressively breaks down or degenerates nerve cells in the brain due to a mutation in the genetic code of a protein called Huntington. This mutation causes defects in the building blocks of DNA due to the repetition of cytosine, adenine, and guanine (CAG) trinucleotides on the short arm of Huntingtin, i.e., HTT (Parsons and Raymond, 2015). This particular HTT gene mutation reduces the growth of the aberrant polyglutamine protein, which causes neurodegeneration (Andhale and Shrivastava, 2022). The nuclear symptoms of this neuropsychiatric disorder include chorea, i.e., abnormal involuntary movements, behavioral and psychiatric disturbances, dementia, and cognitive decline. Patients also have some other psychiatric symptoms including apathy, suicide tendency, mania, and schizophrenia-like symptoms as well as cognitive defects such as lack of attention, motor skill learning deficits, and organizational deficit.

SMA is an autosomal recessive genetic condition affecting muscles that degenerate anterior horn cells, and alpha motoneurons of the spinal cord present symptoms of weakness, wasting, or thinning paralysis of the proximal muscular mass, and significant disability due to low levels of SMN protein in lower spinal cord motor neurons. Reduced levels of SMN have activated the JNK and ROCK signaling pathways in the in vitro and in vivo SMA models (Ahmad et al., 2016). Anterior horn cells are a type of motoneuron emerging from the anterior portion of the gray matter in the spinal cord toward the skeletal muscle, while alpha motoneurons (α) are the lower motoneurons found in the brainstem and spinal cord and are the largest neurons in the spinal cord with myelinated axons. Both are responsible for motor behavior and thus help to generate movement. The term was given by Werdnig and Hoffmann (D’Amico et al., 2011), and the disease could be recognized by the development of symptoms of weakness in one arm and/or one leg as well as facial weakness, numbness or tingling, difficulty in swallowing or speaking, trouble walking and balancing, and gradual memory loss.

Seaweed bioprospecting has garnered significant attention in recent years due to its potential for discovering novel bioactive compounds with diverse applications (Upadhyay and Singh, 2021). Researchers have focused on identifying seaweed species with promising bioactivities and elucidating the chemical structures and biological properties of their components (Donia and Hamann, 2003). Several studies highlighted the neuroprotective effects of seaweed-derived compounds, particularly in the context of neurodegenerative disorders (Olasehinde et al., 2020; Catanesi et al., 2021; Dhahri et al., 2021; Wang et al., 2022; Nyiew et al., 2023). These investigations have underscored the importance of exploring seaweed resources for the development of therapeutic interventions targeting neurological diseases (Schepers et al., 2020). In India, very few regional research efforts have been intensified in the field of neuroprotection, with a particular emphasis on natural products derived from indigenous seaweeds (Suganthy et al., 2010). However, preclinical and clinical investigations conducted have further validated the neuroprotective properties of seaweed-derived agents, paving the way for their potential therapeutic application in neurological disorders. Overall, the convergence of seaweed bioprospecting and neuroprotection research is a growing interest in harnessing marine resources for addressing neurological health challenges, with promising prospects for the development of novel therapeutic interventions.

Polyunsaturated fatty acids (PUFAs) make up between 25% and 60% of total lipids. Phytosterols, glycolipids, phospholipids, and fat-soluble vitamins are among the functional lipid fractions present in seaweeds (carotenoids; vitamins A, D, E, and K), which have relatively low concentrations of lipids (between 1% and 5% of dry weight) (Hamed et al., 2015; Menaa et al., 2020). PUFA-like omega-3-rich foods are pharmacologically significant because they can (i) regulate blood pressure, blood clotting, and membrane fluidity; (ii) lower the risk of diabetes, cardiovascular disease (CVD), and osteoporosis; and (iii) correct the growth and function of the brain and the nervous system (Peng et al., 2015). Isochrysis galbana, Ulva fasciata, Laurencia papillosa, Gracilaria salicornia, Dictyota fasciola, Taonia atomaria, Chaetoceros, Tetraselmis, Thalassiosira, and Nannochloropsis are among the marine algae that are known to produce large amounts of PUFA. Undaria pinnatifida has high concentrations of EPA, DHA, and monounsaturated FAs (C12:1 lauroleic acid, C14:1 myristoleic acid, C16:1 palmitoleic acid, C17:1 cis-10-heptadecenoic acid, and C18:1 oleic acid). Algal lipids also benefit from increased bioavailability and a range of health advantages for both people and animals because of these features. Lipid molecules can combine with glycosidic fragments to form glycolipids, which are categorized into three groups: glycosphingolipids, atypical glycolipids, and glycoglycerol (Cheng-Sánchez and Sarabia, 2018).

Lipids play a major role in PD because they have been found to have anti-inflammatory effects. Omega-3 fatty acids are directly correlated with inducible nitric oxide synthase (iNOS) and hence have a neuroprotective effect on rats. Layé et al. (2018) reported the anti-inflammatory effects of omega-3 fatty acids on microglial and neuronal cells and demonstrated their therapeutic efficacy against neurodegenerative diseases.

Compared to brown seaweed (5%–24%) (such as Sargassum polycystum), edible green seaweed (such as Caulerpa lentillifera) and red seaweed (such as Eucheuma cottonii) have the highest protein content (10%–47% of dry weight) (Peng et al., 2015; Cherry et al., 2019). Significant amounts of proteins are present in Catenella repens, Polysiphonia mollis, Gelidiella acerosa, Capsosiphon fulvescens, Ulva prolifera, Porphyra sp., Osmundea pinnatifida, Pterocladium capillacea, Sphaerococcus coronopifolius, Gelidium microdon, and Cystoseira abies-marin (Cherry et al., 2019).

The prevention and treatment of neurodegenerative diseases, cancers, and gastric ulcers; DNA replication; the response to stimuli; the transport of molecules; and the catalysis of biochemical reactions are all made possible by proteins having anti-inflammatory, antioxidant, antitumor, antiaging, and protective effects (Menaa et al., 2021). Additionally, amino acids are useful in functional medicines, nutraceuticals, and cosmeceuticals since they are used as natural moisturizing agents for hair and skin (Couteau and Coiffard, 2016). Because of their high nutritional value and high protein content, macroalgal species, including Chlorella sp., Dunaliella salina, Aphanizomenon flos-aquae, Dunaliella tertiolecta, and Spirulina platensis, are frequently employed as human food sources (Menaa et al., 2021).

Histidine and taurine are found in Ulva australis; aspartic and glutamic acid (26%–32% of the total amino acids) are found in Ulva spp.; high levels of serine, alanine, and glutamic acid are found in Palmaria palmata (Dulse) and Himanthalia elongata (sea spaghetti); and methionine is found in Sargassum vulgare. Additionally, MAAs have been found in a wide range of species, particularly in Rhodophyta, including Chondrus crispus, Palmaria palmata, Gelidium spp., Porphyra/Pyropia spp., Curdiea racovitzae, Grateloupia lanceola, Asparagopsis armata, Solieria chordalis, and Gracilaria cornea (Menaa et al., 2021).

Additionally, these algal species have the potential to be employed as UV blockers and cell growth stimulants in cosmetics and toiletries (Couteau and Coiffard, 2016). A protein known as phycobilin (i.e., PC and PE) is covalently joined to chromophores to form phycobiliproteins (Cherry et al., 2019). These water-soluble proteins can be employed as natural food colorants and are effective antioxidants. A549 lung cancer cells are resistant to PC, a blue-colored phycobiliprotein mostly generated by the cyanobacterium Arthrospira spp., and PE, a pink-colored protein pigment produced by the cyanobacterium Lyngbya spp. Various proteins, such as carnosine, taurine, and glutathione, demonstrate antiapoptotic and antioxidant effects in the rat brain (Pérez et al., 2016; Pérez-Andrés et al., 2019). Coelho et al. (2017) reported that lectins are glycoproteins that have antinociceptive, antibiotic, mitogenic, and cytotoxic effects.

Carbohydrates or polysaccharides are abundant in several seaweeds and are therapeutically active and have anti-inflammatory and antioxidant effects. Oligosaccharides can be mono- or poly(OH). In brown algae, the monosaccharides present are glucose, galactose, glucuronic acid, mannuronic acid, xylose, and fucose. The polysaccharides used were laminarin, alginate, fucoidan, and mannitol. Red algae include carrageenans, florideans, lignin, and funorans. In addition to these algae, green algae contain ulvan, mannan, xylans, cellulose, and lignin (Barbalace et al., 2019).

Fucoidans, xylans, and ulvans, three minor sulfated polysaccharides, are present in brown, red, and green seaweeds, respectively (Cheong et al., 2018). In Ulva spp., 9% to 36% of the dry mass of algae is made up of sulfated polysaccharides that have been isolated from the intercellular space and the fibrillar wall of green seaweeds (Cherry et al., 2019). Chlorella ellipsoidea has several health advantages, including the ability to improve hemoglobin concentrations, reduce blood sugar levels, and function as a hepatoprotective, neuroprotective, and hypocholesterolemic agent. The most significant component of these goods is β-1,3-glucan, which is a potent immunostimulator, free radical scavenger, and blood lipid reductant (Menaa et al., 2021; Cheong et al., 2018). The ketogenic diet has gained much importance because it contains primarily BHB and ACA, which are used to treat neurological disorders.

The primary polysaccharides of the red algal cell wall, i.e., carrageenans, are categorized into three broad types based on the degree of sulfation: kappa, lambda, and iota (Pérez et al., 2016). Fucoidan polysaccharides are often generated by brown algae such as Sargassum thunbergi, Ascophyllum nodosum, Fucus vesiculosus, Laminaria japonica, Fucus evanescens, and Laminaria cichorioides, which are then exploited to create innovative medications and useful foods (Menaa et al., 2021).

Several studies have investigated the role of saccharides in neurodegeneration. Jin et al. (2017) reported in their study that Gracilaria lemaneiformis extracted from agaro has antioxidant potential when tested on kumming mice. Liu et al. (2019) observed the ability of oligosaccharides from Ulva lactuca and Enteromorpha prolifera to protect brain neurons by reducing oxidative stress and inflammatory factors. Another study by Bi et al. (2020) revealed the neuroprotective effect of seleno-polymannuronate (a selenium derivative of polymannurate) separated from alginate. Selenium is known for guarding neurocytes. He observed the suppression of microglial and astrocytic activation induced by LPS; hence, LPS functions as an anti-neuroinflammatory molecule.

A type of chemical compound known as a phenolic compound has hydroxyl groups that are directly joined to aromatic hydrocarbon rings. The simplest compound is phenol, which has just one aromatic ring. Depending on how many phenol units are present in the molecule, phenolic substances can be either single phenols or polyphenols. All members of the plant kingdom contain phenols in varying amounts, but the phenols found in marine algae are distinct from those made by terrestrial plants (Barbalace et al., 2019). Phenolic acids can easily penetrate the brain and can potentially act on PD, HD, and anti-amyotrophic disease.

Phloroglucinol and phlorotannin are two of the most well-known polyphenols found in marine algae. The subclasses of phlorotannins are eckols, fuhalols, fucophlorethols, phlorethols, fucols, and ishofuhalols. Green and red algae have the most phenolic chemicals (bromophenols, phenolic acids, and flavonoids). The only source of phlorotannins is marine brown algae (Menaa et al., 2021).

Nho et al. (2020) studied the role of phlorotannin from the edible seaweed Ecklonia cava and reported that dickol inhibited AChE and BChE and prolonged acetylcholine neurotransmission in rat brain neurons. Paudel et al. (2019) reported the targeting of eckol from Ecklonia stolonifera and revealed that eckol is an agonist of the dopamine receptor and is active against PD. Rengasamy et al. (2015) concluded that a study on phenolic extracts of Amphiroa beauvoisii, G. foliaceum, Codium capitatum, and C. duthieae revealed a decrease in AChE activity, which was better proven in AD.

Major phytosterol derivatives are found in brown algae, including Agarum cribosum, Undaria pinnatifida, and Laminaria japonica (Menaa et al., 2021). Fucosterol makes up 83%–97% of the total phytosterol concentration. Astaxanthin-carotene, lutein, lycopene, and canthaxanthin are among the many common lipophilic-pigmented molecules known as carotenoids (Bajpai et al., 2018). The antioxidant activity, anti-inflammatory effects, anticancer activity, antiobesity activity, antidiabetic activity, hepatoprotective impact, antiangiogenic effect, and cerebrovascular protective effect are some of the possible health-promoting benefits of these carotenoids.

Fucoxanthin in particular has been shown to reduce oxidative damage and inflammation, and astaxanthin has been shown to reduce IL-6 production in activated microglia (Fantonalgo, 2017), all of which have been linked to the etiology of neurodegenerative disorders.

Various pigments, which impart color, are found in marine algae. Algal color was categorized into three categories: brown pigments from Phaeophyta, green pigments from Chlorophyta (lutein, xanthin, and neoxanthin), and red pigments from Rhodophyta (zeaxanthin). These carotenoids have promising antioxidant and neuroprotective effects (Chuyen and Eun, 2017).

In another study performed by Kim et al. (2017), patients with PD had lower serum levels of alpha and beta carotene, lycopene, and tocopherols than did patients in the control group. Browne et al. (2019) also reported decreased levels of alpha tocopherols and vitamin E in patients with AD. Another study focused on the role of carotenoids in neurodegenerative disorders. Lakey-Beitia et al. (2019) conducted a lead-induced PD study and revealed that treating patients with Crocus sativus hydroethanolic extract prevented all damage to the brain. Furthermore, Fernandes et al. (2021) investigated lutein-loaded nanoparticles in a PD model and found that they had a positive impact on restoring dopamine levels. Lycopene was also found to be more active in AD (C.-B. Liu et al., 2018). Lycopene is involved in downregulating the serum levels of TNF-α and IL-β, hence reducing the inflammatory response at the choroid plexus and improving cognitive defects. Sun et al. (2020) investigated the effect of fucoxanthin on MPTP-induced PD and reported that fucoxanthin counteracted neuronal loss by reducing oxidative stress.

A large number of marine alkaloids can act as neuroprotective agents. Various studies have shown that alkaloids have great potential for treating neurodegenerative disorders. Copmans et al. (2019) reported the specific effects of the isoquinole alkaloids TMC 120 B and TMC 120 B, which were isolated from Aspergillus insuetus, on zebrafish and mice and reported a reduction in seizure duration. Rivanor et al. (2018) investigated the effect of lectin from the green seaweed Caulerpa cupressoides. It reduced the levels of TNF-α and interleukins and hence proved to be a potential anti-inflammatory and antinociceptive agent. Furthermore, Pan et al. (2019) studied the effect of 9-methylfascaplysin from the marine sponge Fascaplysinopsis sp. on a scopolamine-induced AD model, which causes decreased cognitive dysfunction and no Aβ-induced tau hyperphosphorylation.

These compounds are fatty in nature, are obtained from plants, and contribute to maintaining the integrity of biological membranes. Several phytosterols, such as fucosterol and brassicasterol, have been extracted from brown algae, also known as Phaeophyta. In addition, in red algae, also referred to as Rhodophyta, cholesterol is the main principal component, and it has little phytosteroidal content and is composed of fucosterol, desmosterol, chalinasterol, and sitosterol. Poriferasterol, 28-isofucosterol, beta sitosterol, chondrillasterol, and ergosterol are the major phytosterols found in green algae, i.e., chlorophyta. In addition, phytosterols also have anti-inflammatory, antioxidant, and anti-AD effects. Another study revealed the involvement of phytosterols in AD (Wong et al., 2018). He studied several mechanisms of fucosterol’s antioxidant activity, such as an increase in free radical scavenging enzymes and inhibitory activities against AChE, which contribute to AD. Vanbrabant et al. (2021) stated that 24S saringosterol has greater oxidant properties than fucosterol and hence greater neuroprotective power. Several studies have shown the anti-inflammatory potential of fucosterol, which has synergistic effects on neurodegenerative disorders. Alghazwi et al. (2019) reported that seaweed-derived fucoxanthin and fucoidan improve memory deficits. Wong et al. (2018) reported that fucosterol also reduces the generation of inflammatory mediators in Aβ-induced microglia, protecting against Aβ-associated neuroinflammation. Kheiri et al. (2018) reported that the activation of p38 mitogen-activated protein kinase (MAPK) by the Aβ peptide triggers inflammation.

Brown algae are considered to be a renowned source of terpenoids, primarily diterpenes and meroterpenoids. Sargachromenols are the most well-known terpenoids found in Sargassum species. The genus Caulerpa, which is found in green algae, is a source of monocyclic sesquiterpenes and diterpenes with neuroprotective properties (Yang et al., 2014). Many of these compounds contain chromene groups, which may have cytotoxic and antioxidant properties. Three meroterpenoids from S. macrocarpum, sargaquinoic acid, sargahydroquinoic acid, and tuberatolide B have been the subject of previous research. These compounds demonstrated neuroprotective effects, reduced inflammation, and suppressed cancer growth (Gaysinski et al., 2015). Silva et al. (2019) investigated the antioxidant and neuroprotective potential of diterpenes extracted from Bifurcaria bifurcata (brown seaweed). The use of isolated diterpenes has shown promising results in treating PD. Silva also studied the neuroprotective effect of algal extracts on SH-SY5Y cells and found that neurotoxicity was reduced, hence affecting neurodegeneration. Another study on zonarol, a sesquiterpene from the brown algae Dictyopteris undulata, by Shimizu et al. (2015) revealed that zonarol activates the Nrf2/ARE pathway and hence participates in the protection of neuronal cells from oxidative stress. Furthermore, studies by Wozniak et al. (2015) showed the promising effects of Papenfussiella lutea’s extracted sesquiterpenes involved in the inhibition of AChE, hence decreasing AD symptoms. MaChado et al. (2015) reflected the role of halogenated monoterpenes extracted from Ochtodes secundiramea against AD by inhibiting AChE. Recently, Kwon et al. (2022) reported the neuroprotective effects of two monoterpenoid lactones from Sargassum macrocarpum via the inhibition of the MAO enzyme, which is involved in the physiology of PD.