Innate immunity in the Grid2 Lc/+ mouse model of cerebellar neurodegeneration: glial CD95/CD95L plays a non-apoptotic role in persistent neuron loss-associated inflammatory reactions in the cerebellum

Nicotinamide adenine dinucleotide (NAD+) supplies energy for deoxidation and anti-inflammatory reactions fostering the production of adenosine triphosphate (ATP). The kidney is an essential regulator of body fluids through the excretion of numerous metabolites. Chronic kidney disease (CKD) leads to the accumulation of uremic toxins, which induces chronic inflammation. In this study, the role of NAD+ in kidney disease was investigated through the supplementation of nicotinamide (Nam), a precursor of NAD+, to an adenine-induced CKD mouse model. Nam supplementation reduced kidney inflammation and fibrosis and, therefore, prevented the progression of kidney disease. Notably, Nam supplementation also attenuated the accumulation of glycolysis and Krebs cycle metabolites that occurs in renal failure. These effects were due to increased NAD+ supply, which accelerated NAD+-consuming metabolic pathways. Our study suggests that Nam administration may be a novel therapeutic approach for CKD prevention.

Download Full-text

A New Mouse Model Reveals a Critical Role for Host Innate Immunity in Resistance to Rift Valley Fever

The Journal of Immunology ◽

10.4049/jimmunol.1000949 ◽

2010 ◽

Vol 185 (10) ◽

pp. 6146-6156 ◽

Cited By ~ 43

Author(s):

Tânia Zaverucha do Valle ◽

Agnès Billecocq ◽

Laurent Guillemot ◽

Rudi Alberts ◽

Céline Gommet ◽

...

Keyword(s):

Innate Immunity ◽

Mouse Model ◽

Rift Valley ◽

Rift Valley Fever ◽

Critical Role ◽

Valley Fever ◽

Host Innate Immunity

Download Full-text

Effects of sodium methyldithiocarbamate on selected parameters of innate immunity and clearance of bacteria in a mouse model of sepsis

Life Sciences ◽

10.1016/j.lfs.2015.08.001 ◽

2015 ◽

Vol 139 ◽

pp. 1-7 ◽

Cited By ~ 2

Author(s):

Wei Tan ◽

Stephen B. Pruett

Keyword(s):

Innate Immunity ◽

Mouse Model ◽

Sodium Methyldithiocarbamate

Download Full-text

Chronic Memantine Treatment Ameliorates Behavioral Deficits, Neuron Loss, and Impaired Neurogenesis in a Model of Alzheimer’s Disease

Molecular Neurobiology ◽

10.1007/s12035-020-02120-z ◽

2020 ◽

Vol 58 (1) ◽

pp. 204-216

Author(s):

Martina Stazi ◽

Oliver Wirths

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Mouse Model ◽

Recognition Task ◽

Hippocampal Neurogenesis ◽

Adult Hippocampal Neurogenesis ◽

Behavioral Deficits ◽

Neuron Loss ◽

Beneficial Effects ◽

Memantine Treatment

AbstractMemantine, a non-competitive NMDA receptor antagonist possessing neuroprotective properties, belongs to the small group of drugs which have been approved for the treatment of Alzheimer’s disease (AD). While several preclinical studies employing different transgenic AD mouse models have described beneficial effects with regard to rescued behavioral deficits or reduced amyloid plaque pathology, it is largely unknown whether memantine might have beneficial effects on neurodegeneration. In the current study, we assessed whether memantine treatment has an impact on hippocampal neuron loss and associated behavioral deficits in the Tg4-42 mouse model of AD. We demonstrate that a chronic oral memantine treatment for 4 months diminishes hippocampal CA1 neuron loss and rescues learning and memory performance in different behavioral paradigms, such as Morris water maze or a novel object recognition task. Cognitive benefits of chronic memantine treatment were accompanied by an amelioration of impaired adult hippocampal neurogenesis. Taken together, our results demonstrate that memantine successfully counteracts pathological alterations in a preclinical mouse model of AD.

Download Full-text