Neuroprotective Effect of Artemisinin in an Animal Model of Alzheimer's Disease.

Introduction: Alzheimer's disease (AD) is the most common neurodegenerative disease in older people, characterized by the accumulation of beta-amyloid (Aβ) plaques and neurofibrillary tangles composed of aggregated of hyperphosphorylated tau protein, which normally helps stabilize microtubules in neurons.

Method: Nowadays, artemisinin (ART) as well as its semisynthetic derivatives (ARTs) are seen as potential neuroprotectors. The goal of the present study is the assessment of neuroprotective, antibacterial activity of ART, as well as in silico studies of ART affinity to Aβ-peptides and the search of potential targets for ART.

Regulatory effect of bacterial melanin on the isoforms of new superoxide-producing associates from rat tissues in rotenone-induced Parkinson's disease.

According to recent research, selective neuronal vulnerability in Parkinson's disease (PD) results from several phenotypic traits, including calcium-dependent, feed-forward control of mitochondrial respiration leading to elevated reactive oxygen species and cytosolic calcium concentration, an extensive axonal arbor, and a reactive neurotransmitter. Therefore, antioxidant therapy is a promising direction in the treatment of PD. In vitro studies have indicated the survival-promoting activity of bacterial melanin (BM) on midbrain dopaminergic neuron cultures.

Effects of β-amyloid (1-42) Administration on the Main Neurogenic Niches of the Adult Brain: Amyloid-Induced Neurodegeneration Influences Neurogenesis.

Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder and warrants further study as well as timely treatment. Additionally, the mechanisms of the brain's intrinsic defense against chronic injury are not yet fully understood. Herein, we examined the response of the main neurogenic niches to amyloid exposure and the associated changes in structure and synaptic activity.

Assessment of behavioral, morphological and electrophysiological changes in prenatal and postnatal valproate induced rat models of autism spectrum disorder.

Autism spectrum disorders (ASD) are neurodevelopmental disorders, that are characterized by core symptoms, such as alterations of social communication and restrictive or repetitive behavior. The etiology and pathophysiology of disease is still unknown, however, there is a strong interaction between genetic and environmental factors. An intriguing point in autism research is identification the vulnerable time periods of brain development that lack compensatory homeostatic corrections.

The Involvement of Insulin-Like Growth Factor 1 and Nerve Growth Factor in Alzheimer's Disease-Like Pathology and Survival Role of the Mix of Embryonic Proteoglycans: Electrophysiological Fingerprint, Structural Changes and Regulatory Effects on Neurotrophins.

Alzheimer's disease (AD)-associated neurodegeneration is triggered by different fragments of amyloid beta (Aβ). Among them, Aβ (25-35) fragment plays a critical role in the development of neurodegeneration-it reduces synaptic integrity by disruption of excitatory/inhibitory ratio across networks and alters the growth factors synthesis. Thus, in this study, we aimed to identify the involvement of neurotrophic factors-the insulin-like growth factor 1 (IGF-1) and nerve growth factor (NGF)-of AD-like neurodegeneration induced by Aβ (25-35).

Embryonic proteoglycans regulate monoamines in the rat frontal cortex and hippocampus in Alzheimer's disease-like pathology.

Using the rat Alzheimer's disease (AD)-like model we have analyzed the hippocampal short-term potentiation, levels of monoamines, and morphological changes in the hippocampal and cortical neurons after the administration of proteoglycans of embryonic origin (PEG). Results showed that the levels of monoamines and especially norepinephrine in the target AD brain structures were found elevated, except serotonin, which was unaffected in the hippocampus, but decreased in the frontal cortex. These changes were accompanied by the substantial structural damage of cortical and hippocampal neurons.

Alzheimer's disease-like pathology-triggered oxidative stress, alterations in monoamines levels, and structural damage of locus coeruleus neurons are partially recovered by a mix of proteoglycans of embryonic genesis.

Alzheimer's disease (AD) pathogenesis includes oxidative damage and perturbations of monoamines. However, as many details of these alterations are not known, we have investigated the changes in monoamine levels as well as the free radical oxidation processes (FRO) in the brainstem of rats that were administered i.c.