Neuroinflammation is an important feature in the pathogenesis and progression of neurodegenerative diseases such as Alzheimer´s disease (AD), Parkinson´s disease (PD), frontotemporal dementia and amyotrophic lateral sclerosis. Based on current knowledge in the field, suggesting that targeting peripheral inflammation could be a promising additional treatment/prevention approach for neurodegenerative diseases, drugs and natural products with anti-inflammatory properties have been evaluated in animal models of neuroinflammation and neurodegeneration. In this review, we provide an extensive analysis of one of the most important and widely-used animal models of peripherally induced neuroinflammation and neurodegeneration - lipopolysaccharide (LPS)-treated mice, and address the data reproducibility in published research. We also summarize briefly basic features of various natural products, nutraceuticals, with known anti-inflammatory effects and present an overview of data on their therapeutic potential for reducing neuroinflammation in LPS-treated mice.

LPS-induced Murine Neuroinflammation Model: Main Features and Suitability for Pre-clinical Assessment of Nutraceuticals.

The number of the elderly across the globe will approximate 2.1 billion by 2050. Juxtaposed against this burgeoning segment of the population is evidence that nonpathological aging is associated with an increased risk for cognitive decline in a variety of domains, changes that can cause mild disability even before the onset of dementia. Given that pharmacological treatments that mitigate dementia are still outstanding, alternative therapeutic options are being investigated increasingly. The results from translational studies have shown that modifiable lifestyle factors—including physical activity, cognitive engagement, and diet—are a key strategy for maintaining brain health during aging. Indeed, a multiplicity of studies has demonstrated relationships between lifestyle factors, brain structure and function, and cognitive function in aging adults. For example, physical activity and diet modulate common neuroplasticity substrates (neurotrophic signaling, neurogenesis, inflammation, stress response, and antioxidant defense) in the brain whereas cognitive engagement enhances brain and cognitive reserve. The aims of this review are to evaluate the relationship between modifiable lifestyle factors, neuroplasticity, and optimal brain health during aging; to identify putative mechanisms that contribute positive brain aging; and to highlight future directions for scientists and clinicians. Undoubtedly, the translation of cutting-edge knowledge derived from the field of cognitive neuroscience will advance our understanding and enhance clinical treatment interventions as we endeavor to promote brain health during aging.

/pdf/lifestyle-modulators-of-neuroplasticity-how-physical-51az5ghniq.pdf

Lifestyle Modulators of Neuroplasticity: How Physical Activity, Mental Engagement, and Diet Promote Cognitive Health during Aging.

Recent developments in curcumin and curcumin based polymeric materials for biomedical applications: A review.

Behavioral, inflammatory and neurochemical disturbances in LPS and UCMS-induced mouse models of depression.

Physically ill patients with chronic inflammation often present with symptoms of depression. Our understanding of the pathophysiology of inflammation-associated depression has benefited from preclinical studies on the mechanisms of sickness and clinical studies on the symptoms of sickness and depression that develop in patients treated with immunotherapy. Sickness behavior develops when the immune system is activated by pathogen- or damage-associated molecular patterns. It is a normal biological response to infection and cell injury. It helps the organism to mobilize its immune and metabolic defenses to fight the danger. Depression emerges on the background of sickness when the inflammatory response is too intense and long lasting or the resolution process is deficient. The transition from sickness to depression is mediated by activation of the kynurenine metabolism pathway that leads to the formation of neurotoxic kynurenine metabolites including quinolinic acid, an agonist of N-methyl-d-aspartate receptors. The neuroimmune processes and molecular factors that have been identified in the studies of inflammation-associated depression represent potential new targets for the development of innovative therapies for the treatment of major depressive disorders.

/pdf/role-of-the-kynurenine-metabolism-pathway-in-inflammation-iat6gdxdt9.pdf

Role of the kynurenine metabolism pathway in inflammation-induced depression – Preclinical approaches

Resveratrol reverses the effects of chronic unpredictable mild stress on behavior, serum corticosterone levels and BDNF expression in rats.

The effects of curcumin on depressive-like behavior in mice after lipopolysaccharide administration

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Resveratrol reverses the effects of chronic unpredictable mild stress on behavior, serum corticosterone levels and BDNF expression in rats.

The effects of curcumin on depressive-like behavior in mice after lipopolysaccharide administration