Role of de novo lipogenesis in inflammation and insulin resistance in Alzheimer's disease

Khan, Mohsin Ali; Khan, Zaw Ali; Shoeb, Fouzia; Fatima, Ghizal; Khan, Rizwan Hasan; Khan, Mohammad M.

doi:10.1016/j.ijbiomac.2023.124859

Cited by 5 publications

(3 citation statements)

References 86 publications

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“…Unsaturated fatty acids (MUFAs), polyunsaturated fatty acids (PUFAs), and saturated fatty acids (SAFAs) are different types of fatty acids that are components of phospholipids [ 51 ]. Fatty acid imbalances can be a sign of neurological and other mental diseases; elevated levels of SAFAs and MUFAs and decreased levels of PUFAs in the brain tissue are found in AD patients [ 52 ]. A metabolomic study of brain tissue and blood showed that fatty acid biosynthesis is disrupted in clinical AD [ 21 ].…”

Section: Discussionmentioning

confidence: 99%

Metabolic Regulations of Smilax china L. against β-Amyloid Toxicity in Caenorhabditis elegans

Yan,

Deng,

et al. 2024

Metabolites

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Smilax china L. (Chinaroot) is a natural herb that has multiple uses, such as being used to make tea and food. Both its roots and leaves have different uses due to their unique components. In this study, we analyzed the extract of S. china. roots using LC-HRMS and evaluated the neuroprotective effects and metabolic regulation of S. china on Caenorhabditis elegans. Chinaroot extract prolonged the life span of healthy nematodes, delayed the paralysis time of transgenic CL4176, and reduced the level of β-amyloid deposition in transgenic CL2006. The comprehensive analysis of metabolomics and qRT-PCR revealed that Chinaroot extract exerted neuroprotective effects through the valine, leucine and isoleucine degradation and fatty acid degradation pathways. Moreover, we first discovered that the expressions of T09B4.8, ech-7, and agxt-1 were linked to the neuroprotective effects of Chinaroot. The material exerted neuroprotective effects by modulating metabolic abnormalities in AD model C. elegans. Our study provides a new foundation for the development of functional food properties and functions.

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Section: Discussionmentioning

confidence: 99%

Metabolic Regulations of Smilax china L. against β-Amyloid Toxicity in Caenorhabditis elegans

Yan,

Deng,

et al. 2024

Metabolites

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“…30 Peripheral inflammatory mediators, immune and inflammatory cells that cross the BBB, such as mast cells and T cells, as well as pro-inflammatory mediators released by AD microglia cause disruption of the BBB. [31][32][33]…”

Section: The B Lood-b R Ain Barrier (B B B) and Infl Ammationmentioning

confidence: 99%

The neuroinflammatory role of microglia in Alzheimer's disease and their associated therapeutic targets

AmeliMojarad,

AmeliMojarad

2024

CNS Neurosci Ther

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IntroductionAlzheimer's disease (AD), the main cause of dementia, is characterized by synaptic loss and neurodegeneration. Amyloid‐β (Aβ) accumulation, hyperphosphorylation of tau protein, and neurofibrillary tangles (NFTs) in the brain are considered to be the initiating factors of AD. However, this hypothesis falls short of explaining many aspects of AD pathogenesis. Recently, there has been mounting evidence that neuroinflammation plays a key role in the pathophysiology of AD and causes neurodegeneration by over‐activating microglia and releasing inflammatory mediators.MethodsPubMed, Web of Science, EMBASE, and MEDLINE were used for searching and summarizing all the recent publications related to inflammation and its association with Alzheimer's disease.ResultsOur review shows how inflammatory dysregulation influences AD pathology as well as the roles of microglia in neuroinflammation, the possible microglia‐associated therapeutic targets, top neuroinflammatory biomarkers, and anti‐inflammatory drugs that combat inflammation.ConclusionIn conclusion, microglial inflammatory reactions are important factors in AD pathogenesis and need to be discussed in more detail for promising therapeutic strategies.

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“…When there was an excess of Cer in the brain, this pathway could be antagonized. Long-term elevation of Cer in tissues led to sustained impairment of metabolic homeostasis, driving insulin resistance and such kind of damage might be irreversible (120,121). Excess saturated fatty acids in tissues mediated abnormal Cer formation, which further induced endoplasmic reticulum stress, mitochondrial dysfunction and ROS formation, while hypoxia-induced dyshomeostasis of Ca 2+ could also be attributed to increased de novo lipid synthesis and accumulation of saturated fatty acids.…”

Section: Ceramide In Birmentioning

confidence: 99%

Sphingolipid metabolism in brain insulin resistance and neurological diseases

Mei,

Liu,

Mei

et al. 2023

Front. Endocrinol.

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Sphingolipids, as members of the large lipid family, are important components of plasma membrane. Sphingolipids participate in biological signal transduction to regulate various important physiological processes such as cell growth, apoptosis, senescence, and differentiation. Numerous studies have demonstrated that sphingolipids are strongly associated with glucose metabolism and insulin resistance. Insulin resistance, including peripheral insulin resistance and brain insulin resistance, is closely related to the occurrence and development of many metabolic diseases. In addition to metabolic diseases, like type 2 diabetes, brain insulin resistance is also involved in the progression of neurodegenerative diseases including Alzheimer’s disease and Parkinson’s disease. However, the specific mechanism of sphingolipids in brain insulin resistance has not been systematically summarized. This article reviews the involvement of sphingolipids in brain insulin resistance, highlighting the role and molecular biological mechanism of sphingolipid metabolism in cognitive dysfunctions and neuropathological abnormalities of the brain.

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Role of de novo lipogenesis in inflammation and insulin resistance in Alzheimer's disease

Cited by 5 publications

References 86 publications

Metabolic Regulations of Smilax china L. against β-Amyloid Toxicity in Caenorhabditis elegans

Metabolic Regulations of Smilax china L. against β-Amyloid Toxicity in Caenorhabditis elegans

The neuroinflammatory role of microglia in Alzheimer's disease and their associated therapeutic targets

Sphingolipid metabolism in brain insulin resistance and neurological diseases

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