Effects of the <i>Aphanizomenon flos-aquae</i> Extract (Klamin®) on a Neurodegeneration Cellular Model

Nuzzo, Domenico; Presti, Giovanni; Picone, Pasquale; Galizzi, Giacoma; Gulotta, Eleonora; Giuliano, Salvatore; Mannino, C.; Gambino, Vincenzo; Scoglio, Stefano; Carlo, Marta Di

doi:10.1155/2018/9089016

Cited by 35 publications

(35 citation statements)

References 52 publications

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“…Peripheral lipopolysaccharide (LPS) injections in the C57BL/6J mouse led to a prolonged elevated amount of Aβ in the hippocampus with cognitive deficits (Holmes, 2013). Moreover, recent evidences indicate neuroinflammation as an important component of AD pathogenesis (Nuzzo et al, 2014 andNuzzo, Amato, et al, 2018;Nuzzo, Presti, et al, 2018, Pereira et al, 2019, Calsolaro & Edison, 2016).…”

Section: Inflammationmentioning

confidence: 99%

Obesity and Alzheimer’s disease: Molecular bases

Picone

Carlo

Nuzzo

2020

Eur J of Neuroscience

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Obesity is a complex, chronic, and multifactorial condition characterized by abnormal fat accumulation in tissues and organs and inducing negative effects on human health. Alzheimer's disease is a progressive and irreversible neurodegenerative disease, associated with amyloid plaques and neurofibrillary tangles in the brain. The correlation between obesity and Alzheimer's disease has been discovered, but the molecules and molecular mechanisms linking these conditions are not yet fully elucidated. In this review, we focused on the most important processes linking the fat accumulation and the alterations of the brain structure and functions.

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Section: Inflammationmentioning

confidence: 99%

Obesity and Alzheimer’s disease: Molecular bases

Picone

Carlo

Nuzzo

2020

Eur J of Neuroscience

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“…VA has also been shown to have significant antioxidant capabilities. An extract derived from Aphanizomenon flos-aquae cyanobacteria, of which VA is a major component, significantly protected a neuroblastoma cell line from tert-butylhydroperoxide-induced oxidative stress [184]. Moreover VA was shown to significantly reduce oxidative stress induced by hydrogen peroxide and preserve cellular viability in the SH-SY5Y neuronal cell line through elevated expression of several antioxidant enzymes and pro-survival signaling pathways [185].…”

Section: The Use Of Anthocyanin Metabolites As Novel Neuroprotectimentioning

confidence: 99%

“…GA has also been demonstrated to increase calbindin expression, a marker of preserved calcium homeostasis, in primary cortical neurons challenged with glutamate [183]. An extract rich in VA has also shown positive effects in the context of amyloid beta toxicity in a neuroblastoma cell line, preventing oxidative stress, and blunting the inflammatory effects of this insult by decreasing NF-κB activation and inflammatory cytokine expression [184]. These observations were confirmed in HT22 cells treated with amyloid beta and pure VA [200].…”

Section: The Use Of Anthocyanin Metabolites As Novel Neuroprotectimentioning

confidence: 99%

Anthocyanins and Their Metabolites as Therapeutic Agents for Neurodegenerative Disease

2019

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Neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis (ALS), are characterized by the death of neurons within specific regions of the brain or spinal cord. While the etiology of many neurodegenerative diseases remains elusive, several factors are thought to contribute to the neurodegenerative process, such as oxidative and nitrosative stress, excitotoxicity, endoplasmic reticulum stress, protein aggregation, and neuroinflammation. These processes culminate in the death of vulnerable neuronal populations, which manifests symptomatically as cognitive and/or motor impairments. Until recently, most treatments for these disorders have targeted single aspects of disease pathology; however, this strategy has proved largely ineffective, and focus has now turned towards therapeutics which target multiple aspects underlying neurodegeneration. Anthocyanins are unique flavonoid compounds that have been shown to modulate several of the factors contributing to neuronal death, and interest in their use as therapeutics for neurodegeneration has grown in recent years. Additionally, due to observations that the bioavailability of anthocyanins is low relative to that of their metabolites, it has been proposed that anthocyanin metabolites may play a significant part in mediating the beneficial effects of an anthocyanin-rich diet. Thus, in this review, we will explore the evidence evaluating the neuroprotective and therapeutic potential of anthocyanins and their common metabolites for treating neurodegenerative diseases.

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“…In particular, AFA extract interfered with Aβ aggregation by inhibiting its extension, producing aggregates of shorter dimensions, and destabilizing the preformed fibrils. Furthermore, the AFA extract exerted anti-inflammatory activity consequent to Aβ toxic stimulus, decreasing the production of proinflammatory cytokines such as IL-6 and IL-1β [140,141].…”

Section: New Frontiers In Nutritional Prevention: Microalgal-derived mentioning

confidence: 99%

Natural Compounds as Beneficial Antioxidant Agents in Neurodegenerative Disorders: A Focus on Alzheimer’s Disease

2019

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The positive role of nutrition in chronic neurodegenerative diseases (NDs) suggests that dietary interventions represent helpful tools for preventing NDs. In particular, diets enriched with natural compounds have become an increasingly attractive, non-invasive, and inexpensive option to support a healthy brain and to potentially treat NDs. Bioactive compounds found in vegetables or microalgae possess special properties able to counteract oxidative stress, which is involved as a triggering factor in neurodegeneration. Here, we briefly review the relevant experimental data on curcuminoids, silymarin, chlorogenic acid, and compounds derived from the microalga Aphanizomenon flos aquae (AFA) which have been demonstrated to possess encouraging beneficial effects on neurodegeneration, in particular on Alzheimer's disease models. and intracellular neurofibrillary tangles (NFTs) [4,5]. Intracellular neurofibrillary tangles are composed of hyperphosphorylated Tau proteins in neurons located particularly in the hippocampus and cerebral cortex regions of the brain. The reduced expression of the brain-derived neurotrophic factor (BDNF), important for neuronal growth and memory functions, also plays a crucial role in AD pathogenesis via formation of senile plaque of Aβ and NFTs. At the molecular level, Aβ induces oxidative stress, inflammation, and mitochondrial dysfunction associated with apoptosis [6,7].Parkinson's disease is characterized by the progressive loss of dopaminergic neurons in the substantia nigra (SN) and formation of Lewy bodies, abnormal intraneuronal aggregates of proteins that include α-synuclein, ubiquitin, and neurofilaments [8]. The pathogenic mechanisms of PD include oxidative stress, mitochondrial and protein dysfunction, inflammation, and apoptosis [9]. In particular, oxidative stress generates ROS which activates glial cells, and activated glial cells generate inflammation that results in mitochondrial dysfunction, and, consequently, dysfunctional mitochondria activate cell death machinery [10].Hence, oxidative stress and mitochondrial damage are common factors involved in the etiopathology of these neurodegenerative diseases [11-13]. Oxidative Stress and NeurodegenerationOxidative stress is characterized by an overproduction of ROS-oxygen-containing molecules known to be highly reactive.Reactive oxygen species are formed in mitochondria during oxidative phosphorylation as a byproduct of normal metabolism. Therefore, modest levels of ROS are normally expected and are considered essential for the regulation of normal cell functions, while excessive ROS production can damage various biological targets, such as DNA, lipids, and proteins, causing serious neurological injury. Because the brain consumes a large amount of molecular oxygen to function properly, the accumulation of damaged biomolecules caused by ROS is high, especially with aging [14]. To limit these cellular damages, brain neurons produce antioxidant defense enzymes, such as superoxide dismutase (SOD), glutathione peroxidase (GPX) and catala...

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Effects of the Aphanizomenon flos-aquae Extract (Klamin®) on a Neurodegeneration Cellular Model

Cited by 35 publications

References 52 publications

Obesity and Alzheimer’s disease: Molecular bases

Obesity and Alzheimer’s disease: Molecular bases

Anthocyanins and Their Metabolites as Therapeutic Agents for Neurodegenerative Disease

Natural Compounds as Beneficial Antioxidant Agents in Neurodegenerative Disorders: A Focus on Alzheimer’s Disease

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