Abstract
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.
Highlights
Chronic neurodegenerative diseases (NDs), such as dementia and its most frequent etiological types—Alzheimer’s disease (AD) and Parkinson’s Disease (PD), are a growing cause of disability and death, characterized by progressive loss or dysfunction of neurons in specific areas of the brain.Patients with these disorders display variable clinical features including cognitive decline, speech difficulties, and motor impairment [1]
A recent work [20] showed that, in the brains of mice fed with a hyperglycemic diet (HGD) or high-fat diet (HFD), changes occurred in the phosphorylation of proteins involved in synaptic plasticity and neuronal functionality
This review summarizes the neuroprotective activities of curcuminoids, silymarin, and chlorogenic acids, for which we recently explored the beneficial properties in preventing obesity-related neurodegeneration [57]
Summary
Chronic neurodegenerative diseases (NDs), such as dementia and its most frequent etiological types—Alzheimer’s disease (AD) and Parkinson’s Disease (PD), are a growing cause of disability and death, characterized by progressive loss or dysfunction of neurons in specific areas of the brain. Patients with these disorders display variable clinical features including cognitive decline, speech difficulties, and motor impairment [1]. The reduced expression of the brain-derived neurotrophic factor (BDNF), important for neuronal growth and memory functions, 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]. Oxidative stress and mitochondrial damage are common factors involved in the etiopathology of these neurodegenerative diseases [11,12,13]
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