Tag: neuroinflammation

Molecular approaches to the treatment, prophylaxis, and diagnosis of Alzheimer’s disease: endoplasmic reticulum stress and immunological stress in pathogenesis of Alzheimer’s disease

This review explores the roles of endoplasmic reticulum (ER) stress and immunological stress in Alzheimer’s disease (AD) pathogenesis. ER stress, resulting from the accumulation of misfolded proteins, activates the unfolded protein response (UPR), which aims to restore protein homeostasis but can lead to apoptosis if prolonged. Key UPR pathways involve

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Progesterone suppresses Aβ-induced neuroinflammation by enhancing autophagy in astrocytes

This study investigates the neuroprotective effects of progesterone (PG) against amyloid-beta (Aβ42)-induced neuroinflammation in astrocytes. The findings reveal that Aβ42 impairs autophagic processes in astrocytes, leading to increased inflammatory responses. Treatment with PG significantly enhances autophagy activation, as evidenced by upregulation of autophagy markers and modulation of the mTOR signaling

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The Pivotal Role of Nitric Oxide: Effects on the Nervous and Immune Systems

This 2014 review explores nitric oxide (NO) as a critical signaling molecule with dual roles in physiological and pathological processes within the nervous and immune systems. In the nervous system, NO functions as a neurotransmitter and neuromodulator, influencing synaptic plasticity, neurovascular coupling, and mitochondrial biogenesis. Conversely, excessive NO production can

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Multiple Mechanisms Linking Type 2 Diabetes and Alzheimer’s Disease: Testosterone as a Modifier

This 2017 review explores the interconnected pathophysiology of type 2 diabetes mellitus (T2DM) and Alzheimer’s disease (AD), highlighting shared mechanisms such as insulin resistance, lipid dysregulation, inflammation, and oxidative stress. The authors propose that low testosterone levels may exacerbate these conditions by impairing insulin signaling, increasing amyloid-β accumulation, and promoting

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Functional Food Nutrients, Redox Resilience Signaling and Neurosteroids for Brain Health

This systematic review explores the role of functional food nutrients, such as flavonoids (curcumin, resveratrol), probiotics, vitamin D, and omega-3 fatty acids, in enhancing brain health by modulating oxidative stress and neuroinflammation through the Nrf2 antioxidant pathway. These nutrients activate protective genes like HO-1 and Sirt1, helping to maintain neurosteroid

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GluR2 can Drive Neuroinflammation and Cognitive Impairments Following Peripherally Repeated Lipopolysaccharide Exposures

This study demonstrated that GluR2 plays a key role in neuroinflammation and cognitive impairments in a mouse model exposed to repeated peripheral lipopolysaccharide (LPS). LPS exposure led to cognitive deficits, microglial activation, increased GluR1 and GluR2 levels, and reduced synaptic integrity in the hippocampus. The AMPA receptor antagonist CFM-2 and

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Lipopolysaccharides (LPSs) as Potent Neurotoxic Glycolipids in Alzheimer’s Disease (AD)

This 2022 review published in the International Journal of Molecular Sciences (DOI: 10.3390/ijms232012671) explores how lipopolysaccharides (LPSs) from Gram-negative gut bacteria contribute to the pathogenesis of Alzheimer’s disease (AD). The article details how LPSs can translocate into systemic circulation through compromised gut and blood-brain barriers—especially in aging or those with

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LPS induces microglial activation and GABAergic synaptic deficits in the hippocampus accompanied by prolonged cognitive impairment

This 2023 in vivo animal study published in Scientific Reports (DOI: 10.1038/s41598-023-32798-9) explored how systemic inflammation induced by lipopolysaccharide (LPS) affects microglial activation, synaptic function, and cognition. Using a mouse model, researchers found that microglial activation peaked 3 days after LPS injection and was followed by GABAergic synaptic impairments and

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Neuroinflammation induced by lipopolysaccharide causes cognitive impairment in mice

This 2019 in vivo study published in Scientific Reports (DOI: 10.1038/s41598-019-42286-8) explored the effects of lipopolysaccharide (LPS)-induced neuroinflammation on cognition in mice. LPS administration activated microglia, increased pro-inflammatory cytokines (TNF-α, IL-1β), decreased anti-inflammatory cytokines (IL-4, IL-10), and impaired memory performance in behavioral tests. It also triggered NF-κB pathway activation and

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