Neurochemical Aspects of Neurodegenerative Diseases

Farooqui, Akhlaq A.

doi:10.1007/978-1-4419-6652-0_8

Cited by 9 publications

(15 citation statements)

References 313 publications

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“…The molecular mechanism associated with loss of synapse and decrease in plasmalogens is not yet fully understood. However, it is proposed that Aβ oligomers induce stimulation of plasmalogen-selective PLA 2 (PlsEtn-PLA 2 ) and may be responsible for the decrease in plasmalogen levels and synaptic loss in AD (Farooqui, 2010a;Farooqui, 2010b;Farooqui, 2012a). Since plasmalogens are essential structural phospholipids of synapses and neurons, decreases in plasmalogen pools may likely be responsible for the loss of synapse and the shrinkage of neurons that precedes neurodegeneration in AD.…”

Section: Dha-derived Protectins and Neuroprotectinsmentioning

confidence: 98%

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n-3 Fatty Acid-Derived Lipid Mediators against Neurological Oxidative Stress and Neuroinflammation

Farooqui¹

2014

Omega-3 Fatty Acids in Brain and Neurological Health

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Section: Dha-derived Protectins and Neuroprotectinsmentioning

confidence: 98%

“…DHA and its metabolites also suppress several signal transduction pathways induced by Aβ, including two major kinases that phosphorylate the microtubule-associated protein tau and promote neurofibrillary tangle pathology (Farooqui, 2009;Farooqui, 2010a) (Table 7.1).…”

Section: Dha-derived Protectins and Neuroprotectinsmentioning

confidence: 98%

n-3 Fatty Acid-Derived Lipid Mediators against Neurological Oxidative Stress and Neuroinflammation

Farooqui¹

2014

Omega-3 Fatty Acids in Brain and Neurological Health

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“…All these studies indicate some biochemical features of MetS, such as an impairment of antioxidant systems and increase in lipid peroxidation products during an episode of stroke [131,132] and of inflammatory status [153]. In addition, at the cellular and molecular level, insulin resistance confers changes that play important role in the pathophysiology of vascular diseases, including stroke.…”

Section: Metabolic Syndrome and Strokementioning

confidence: 99%

“…Metabolic syndrome and Alzheimer's disease AD is a multifactorial disease characterized by progressive neuronal degeneration, gliosis, and accumulation of senile plaques (SP) and neurofibrillary tangles (NPT), which are aggregates of amyloid-b (Ab) peptides derived from proteolytic cleavages of amyloid precursor protein (APP) and hyperphosphorylated tau protein, respectively [153]. The aggregation of Ab is the result of an abnormal amyloid precursor protein (APP) cleavage by b-and c-secretases.…”

Section: Metabolic Syndrome and Strokementioning

confidence: 99%

“…The aggregation of Ab is the result of an abnormal amyloid precursor protein (APP) cleavage by b-and c-secretases. In addition, impairment in energy metabolism, mitochondrial dysfunction and alterations in neural membrane phospholipid, sphingolipid and cholesterol levels have also been reported in AD [153]. Type II diabetes mellitus is associated with an increased risk of cognitive dysfunction and AD [149,164].…”

Section: Metabolic Syndrome and Strokementioning

confidence: 99%

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Metabolic syndrome as a risk factor for neurological disorders

Farooqui

Panza

et al. 2011

Cell. Mol. Life Sci.

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171

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The metabolic syndrome is a cluster of common pathologies: abdominal obesity linked to an excess of visceral fat, insulin resistance, dyslipidemia and hypertension. At the molecular level, metabolic syndrome is accompanied not only by dysregulation in the expression of adipokines (cytokines and chemokines), but also by alterations in levels of leptin, a peptide hormone released by white adipose tissue. These changes modulate immune response and inflammation that lead to alterations in the hypothalamic 'bodyweight/appetite/satiety set point,' resulting in the initiation and development of metabolic syndrome. Metabolic syndrome is a risk factor for neurological disorders such as stroke, depression and Alzheimer's disease. The molecular mechanism underlying the mirror relationship between metabolic syndrome and neurological disorders is not fully understood. However, it is becoming increasingly evident that all cellular and biochemical alterations observed in metabolic syndrome like impairment of endothelial cell function, abnormality in essential fatty acid metabolism and alterations in lipid mediators along with abnormal insulin/leptin signaling may represent a pathological bridge between metabolic syndrome and neurological disorders such as stroke, Alzheimer's disease and depression. The purpose of this review is not only to describe the involvement of brain in the pathogenesis of metabolic syndrome, but also to link the pathogenesis of metabolic syndrome with neurochemical changes in stroke, Alzheimer's disease and depression to a wider audience of neuroscientists with the hope that this discussion will initiate more studies on the relationship between metabolic syndrome and neurological disorders.

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