Current research is geared towards the discovery of new compounds with strong neuroprotective potential and few or no side effects compared to synthetic drugs. This review focuses on the potentials of extracts and biologically active compounds derived from microalgal biomass for the treatment and management of Alzheimer’s disease (AD). Microalgal research has gained much attention recently due to its contribution to the production of renewable fuels and the ability of alga cells to produce several secondary metabolites such as carotenoids, polyphenols, sterols, polyunsaturated fatty acids and polysaccharides. These compounds exhibit several pharmacological activities and possess neuroprotective potential. The pathogenesis of Alzheimer’s disease (AD) involves complex mechanisms that are associated with oxidative stress, cholinergic dysfunction, neuronal damage, protein misfolding and aggregation. The antioxidant, anticholinesterase activities as well as the inhibitory effects of some bioactive compounds from microalgae extracts on β-amyloid aggregation and neuronal death are discussed extensively. Phytochemical compounds from microalgae are used as pharmaceuticals, nutraceuticals and food supplements, and may possess neuroprotective potentials that are relevant to the management and/or treatment of AD.

Several studies present the neurotoxic effects of polycyclic aromatic hydrocarbons (PAHs), a class of environmental pollutants capable of causing neurological deficits. However, a collective review approach to this research topic is scarce. This study presents the effect of PAHs on the central nervous system using a bibliometric approach. The neuropathological mechanisms of PAHs are also highlighted. Published articles were searched for in the Scopus and Web of Science databases from January 1979 to December 2020 using the keywords ‘polycyclic aromatic hydrocarbons’ and ‘neurotoxicity’. The total number of documents retrieved from both databases was 338. Duplicated documents (80) were excluded and 258 articles were used for the final analysis. Our findings revealed that there has been a significant increase in research outputs on this topic in the last ten years. The countries with the highest scientific productivity in this area are USA, China, France and Italy. The result also showed that, in the past few years, global scientific output in research relating to PAH neurotoxicity focused on neurodegeneration, cholinergic function, neurodevelopmental toxicity, behavioural studies, oxidative stress, neuroprotection and therapeutic intervention using different experimental models, including zebrafish, neuronal cell lines, Caenorhabditis elegans and rats. Recent studies also revealed the neuroprotective roles of some natural products against PAH-induced neurotoxicity. However, more investigation involving clinical trials is required to emphasize the observed neurotoxic effects.

This study was designed to determine the antioxidant properties and inhibitory effects of extract fromMoringa oleiferaleaves on angiotensin-I-converting enzyme (ACE) and arginase activitiesin vitro. The extract was prepared and phenolic (total phenols and flavonoid) contents, radical (nitric oxide (NO), hydroxyl (OH)) scavenging abilities, and Fe²⁺-chelating ability were assessed. Characterization of the phenolic constituents was done via high performance liquid chromatography-diode array detection (HPLC-DAD) analysis. Furthermore, the effects of the extract on Fe²⁺-induced MDA production in rats’ penile tissue homogenate as well as its action on ACE and arginase activities were also determined. The extract scavengedNO∗,OH∗, chelated Fe²⁺, and inhibited MDA production in a dose-dependent pattern with IC₅₀values of 1.36, 0.52, and 0.38 mg/mL and 194.23 µg/mL, respectively. Gallic acid, chlorogenic acid, quercetin, and kaempferol were the most abundant phenolic compounds identified in the leaf extract. The extract also inhibited ACE and arginase activities in a dose-dependent pattern and their IC₅₀values were 303.03 and 159.59 µg/mL, respectively. The phenolic contents, inhibition of ACE, arginase, and Fe²⁺-induced MDA production, and radical (OH∗,NO∗) scavenging and Fe²⁺-chelating abilities could be some of the possible mechanisms by whichM. oleiferaleaves could be used in the treatment and/or management of erectile dysfunction.

This study was designed to evaluate the antioxidant and cholinesterase inhibitory activities of sulfated polysaccharides from Gracilaria gracilis (PGCL) and Ulva lactuca (PULV). PGCL and PULV were extracted and characterized with Scanning electron microscope-energy dispersive x-ray (SEM-EDX), Fourier transform infrared spectroscopy (FTIR) and Gas chromatography-mass spectroscopy (GC-MS). The radical (2,2-azinobis-3-ethylbenzothiazoline-6-sulfonate [ABTS] 2,2-diphenyl-1- picrylhydrazyl [DPPH], and hydroxyl [OH]) scavenging and metal chelating activities as well as their inhibitory effects on acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) activities were also determined. SEM-EDX analysis revealed the presence of elements such as carbon, magnesium, calcium, phosphorus, and sulfur. The FTIR analysis also confirmed the presence of sulfate group in the polysaccharide samples. Some sugars such as glucose, galactose, arabinose, xylose, rhamnose, and allose were also identified using GC-MS. PGCL and PULV scavenged ABTS, DPPH and OH radicals in a dose-dependent manner. Moreover, PULV exhibited higher scavenging activity compared to PGCL. PGCL and PULV also reduced the activity of AChE (IC₅₀ = 132.73 and 106.93 µg/mL) and BChE (IC₅₀ = 124.93 and 93.45 µg/mL) respectively. PGCL and PULV exhibited antioxidant activity and possess cholinesterase inhibitory activity, hence these polysaccharides could be explored as ingredients for the development of functional foods with neuroprotective potentials.

Alzheimer’s disease (AD) is a neurological condition that affects mostly aged individuals. Evidence suggests that pathological mechanisms involved in the development of AD are associated with cholinergic deficit, glutamate excitotoxicity, beta-amyloid aggregation, tau phosphorylation, neuro-inflammation, and oxidative damage to neurons. Currently there is no cure for AD; however, synthetic therapies have been developed to effectively manage some of the symptoms at the early stage of the disease. Natural products from plants and marine organisms have been identified as important sources of bioactive compounds with neuroprotective potentials and less adverse effects compared to synthetic agents. Seaweeds contain several kinds of secondary metabolites such as phlorotannins, carotenoids, sterols, fucoidans, and poly unsaturated fatty acids. However, their neuroprotective effects and mechanisms of action have not been fully explored. This review discusses recent investigations and/or updates on interactions of bioactive compounds from seaweeds with biomarkers involved in the pathogenesis of AD using reports in electronic databases such as Web of science, Scopus, PubMed, Science direct, Scifinder, Taylor and Francis, Wiley, Springer, and Google scholar between 2015 and 2019. Phlorotannins, fucoidans, sterols, and carotenoids showed strong neuroprotective potentials in different experimental models. However, there are no data from human studies and/or clinical trials.

This study was designed to evaluate and compare the interactions of essential oils from orange (Citrus sinensis [L.] Osbeck) and lemon (Citrus limon) peels on enzymes linked to type-2 diabetes (α-amylase and α-glucosidase) and hypertension (angiotensin-I-converting enzyme [ACE]). The essential oils were obtained from the peels by hydrodistillation and were passed over anhydrous sodium sulphate. The interaction of the oil on α-amylase, α-glucosidase, and ACE activities was subsequently determined. The results revealed that the essential oils inhibited α-amylase and α-glucosidase activities. However, lemon peel (IC₅₀ = 8.16 µg/mL and 7.56 µg/mL) essential oil exhibited stronger inhibitory activity on α-amylase and α-glucosidase activities compared to orange peels (IC₅₀ = 11.51 µg/mL and 11.53 µg/mL), respectively. Similarly, both essential oils reduced the activity of ACE. Moreover, lemon peel (IC₅₀ = 26.17 µg/mL) essential oil showed higher inhibitory effect compared to orange peel (IC₅₀ = 31.79 µg/mL). Our findings revealed that essential oils from lemon and orange peels are potential antidiabetic and antihypertensive agents. Moreover, essential oil from lemon peels was more potent than orange peels.