Lipids Nutrients in Parkinson and Alzheimer’s Diseases: Cell Death and Cytoprotection

Abstract

Neurodegenerative diseases, particularly Parkinson’s and Alzheimer’s, have common features: protein accumulation, cell death with mitochondrial involvement and oxidative stress. Patients are treated to cure the symptoms, but the treatments do not target the causes; so, the disease is not stopped. It is interesting to look at the side of nutrition which could help prevent the first signs of the disease or slow its progression in addition to existing therapeutic strategies. Lipids, whether in the form of vegetable or animal oils or in the form of fatty acids, could be incorporated into diets with the aim of preventing neurodegenerative diseases. These different lipids can inhibit the cytotoxicity induced during the pathology, whether at the level of mitochondria, oxidative stress or apoptosis and inflammation. The conclusions of the various studies cited are oriented towards the preventive use of oils or fatty acids. The future of these lipids that can be used in therapy/prevention will undoubtedly involve a better delivery to the body and to the brain by utilizing lipid encapsulation.

Beneficial Effects of Citrus-Derived Polymethoxylated Flavones for Central Nervous System Disorders

“…Central nervous system disorders have numerous pathological similarities at the sub-cellular and molecular levels, including oxidative stress, neuroinflammation, and memory impairment [ 7 , 8 , 87 , 88 , 89 ]. All these processes increase in the aging brain [ 90 ].…”

Prevention of 7-Ketocholesterol-Induced Overproduction of Reactive Oxygen Species, Mitochondrial Dysfunction and Cell Death with Major Nutrients (Polyphenols, ω3 and ω9 Unsaturated Fatty Acids) of the Mediterranean Diet on N2a Neuronal Cells

“…In Parkinson's and Alzheimer's disease, protein aggregation and mitochondrial dysfunction are two factors that promote oxidative stress, which is considered a major element in the evolution of these diseases [1]. In Parkinson's disease, at the level of substancia nigra pars compacta, α-synuclein aggregates (Lewy bodies) induce a degeneration of dopaminergic neurons involving oxidative stress [1].…”

“…In Parkinson's and Alzheimer's disease, protein aggregation and mitochondrial dysfunction are two factors that promote oxidative stress, which is considered a major element in the evolution of these diseases [1]. In Parkinson's disease, at the level of substancia nigra pars compacta, α-synuclein aggregates (Lewy bodies) induce a degeneration of dopaminergic neurons involving oxidative stress [1]. In Alzheimer's disease, the increase in oxidative stress mediated by β-amyloid protein aggregates (senile plaques) in the hippocampus and cortex promotes excitotoxicity (pathological process by which nerve cells are damaged or killed by excessive stimulation by neurotransmitters) and synaptic degeneration leading to neurodegeneration [1].…”

“…In Parkinson's disease, at the level of substancia nigra pars compacta, α-synuclein aggregates (Lewy bodies) induce a degeneration of dopaminergic neurons involving oxidative stress [1]. In Alzheimer's disease, the increase in oxidative stress mediated by β-amyloid protein aggregates (senile plaques) in the hippocampus and cortex promotes excitotoxicity (pathological process by which nerve cells are damaged or killed by excessive stimulation by neurotransmitters) and synaptic degeneration leading to neurodegeneration [1]. Identifying natural or synthetic molecules that could prevent oxidative stress is therefore a part of therapeutic strategies for treatment of Parkinson's and Alzheimer's diseases.…”

“…Identifying natural or synthetic molecules that could prevent oxidative stress is therefore a part of therapeutic strategies for treatment of Parkinson's and Alzheimer's diseases. Among the molecules already identified are neuropeptides and natural antioxidants which have both antioxidant and/or anti-aggregation properties [1][2][3]. Furthermore, one of the consequences of oxidative stress is to promote the formation of lipid derivatives, including oxidized cholesterol derivatives (oxysterols) such as 7-ketocholesterol (7KC, also named 7-oxocholesterol) and 7β-hydroxycholesterol [4][5][6], which contribute to amplifying the oxidative stress that promotes inflammation and cell death, two other important components of neurodegeneration [7].…”