Background: Parkinson's disease (PD) has been described in dopamine brain level reductions. Conversely, several studies have shown that parasite can increase the level of dopamine in an infected host. This study was conducted to assess the serum, cerebral dopamine levels, and downregulation of Parkinson's disease manifestations in mice with chronic toxoplasmosis.
Methods: PD induction was done by oral inoculation of rotenone into BALB/c mice. To induce the chronic infection, cysts of Prugniaud strain (genotype II) were injected intraperitoneally into the mice. The rotarod test was used for the evaluation of functional motor disorders in experimental mice. The serum and cerebral dopamine levels of the mice were also measured by using high-performance liquid chromatography (HPLC) on consecutive periods (10 days).
Results: Findings of the rotarod test showed the highest and lowest average of running duration belonged to the uninfected mice and PD mice, respectively. Remarkably, the running duration of infected mice with PD was higher than PD mice. As well, the level of serum and cerebral dopamine increased in mice with PD and toxoplasmosis in comparison with PD mice.
Conclusion: Increasing the serum and cerebral dopamine levels in mice infected with toxoplasmosis is related to the presence of the parasite. Moreover, the dopamine upregulation due to the infection is effective in the reduction of PD complications.
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http://dx.doi.org/10.1155/2022/5716765 | DOI Listing |
Background: Senile dementia (SD) is a deteriorative organic brain disorder and it comprises Alzheimer's disease (AD) as a major variant. SD is shown impairment of mental capacities whereas AD is degeneration of neurons. According to World Health Organization (WHO) report; more than 55 million peoples have dementia and it is raising 10 million new cases every year.
View Article and Find Full Text PDFBackground: Abnormal glucose metabolism in AD brains correlates with cognitive deficits. The glucose changes are consistent with brain thiamine (vitamin B1) deficiency. In animals, thiamine deficiency causes multiple AD-like changes including memory loss, neuron loss, brain inflammation, enhanced phosphorylation of tau, exaggerated plaque formation and elevated advanced glycation end products (AGE).
View Article and Find Full Text PDFBackground: A large body of evidence now indicates that the most pathogenic species of Aß in Alzheimer's disease (AD) consist of soluble toxic oligomers (AßO) as opposed to insoluble fibrils and monomers. Using our computational platform, we identified 4 different AßO-restricted conformational B cell epitopes (300, 301, 303, 305) that were tested as vaccines for their ability to induce an antibody response that selectively targets toxic AßO, without inducing potentially detrimental B or T cell responses against plaque or normal Aß. A novel ex vivo approach was then used to select an optimal vaccine configuration amongst the 15 possible combinations of the 4 epitopes to provide maximal binding to a toxic oligomer-enriched low molecular weight (LMW) fraction of soluble AD brain extracts.
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December 2024
L & J Bio, Co., Ltd, Seoul, Songpa-Gu, Korea, Republic of (South).
Background: Neurofibrillary tangles (NFTs), along with amyloid beta plaque, are neuropathological aggregates of Alzheimer's Disease (AD). Hyperphosphorylated tau is responsible for the NFTs formation and further neurodegeneration in AD. The hippocampal region and the entorhinal cortex (EC) have been a major focus of AD research because the deposits of hyperphosphorylated tau protein and NFT in these regions are correlated with memory deficits.
View Article and Find Full Text PDFBackground: VY-TAU01 is a recombinant humanized IgG4 monoclonal antibody (mAb) directed against pathological tau for the treatment of patients with mild dementia or mild cognitive impairment due to Alzheimer's disease (AD). Both VY-TAU01 and its parental mouse IgG1 mAb Ab-01 target an epitope in the C-terminus of tau, bind pathological tau with high affinity and selectivity over wild-type tau, block paired helical filament seed-induced tau aggregates in vitro, and selectively stain tau tangles in AD and P301S mouse (C57/B6J-Tg[Thy1-MAPT*P301S]2541Godt) brain. Ab-01 robustly inhibits seeding and propagation of pathological tau in a P301S mouse seeding model.
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