Brain-derived neurotrophic factor (BDNF) promotes neuroprotection and neuroregeneration. In animal models of Parkinson’s disease (PD), BDNF enhances the survival of dopaminergic neurons, improves dopaminergic neurotransmission and motor performance. Pharmacological therapies of PD are symptom-targeting, and their effectiveness decreases with the progression of the disease; therefore, new therapeutical approaches are needed. Since, in both PD patients and animal PD models, decreased level of BDNF was found in the nigrostriatal pathway, it has been hypothesized that BDNF may serve as a therapeutic agent. Direct delivery of exogenous BDNF into the patient’s brain did not relieve the symptoms of disease, nor did attempts to enhance BDNF expression with gene therapy. Physical training was neuroprotective in animal models of PD. This effect is mediated, at least partly, by BDNF. Animal studies revealed that physical activity increases BDNF and tropomyosin receptor kinase B (TrkB) expression, leading to inhibition of neurodegeneration through induction of transcription factors and expression of genes related to neuronal proliferation, survival, and inflammatory response. This review focuses on the evidence that increasing BDNF level due to gene modulation or physical exercise has a neuroprotective effect and could be considered as adjunctive therapy in PD.

Increase in oxidative stress has been postulated to play an important role in the pathogenesis of a number of neurodegenerative diseases including Alzheimer’s disease. There is evidence for involvement of amyloid‐β peptide (Aβ) in mediating the oxidative damage to neurons. Despite yet unknown mechanism, Aβ appears to exert action on the ionotropic glutamate receptors, especially the N‐methyl‐D‐aspartic acid (NMDA) receptor subtypes. In this study, we showed that NMDA and oligomeric Aβ_1–42 could induce reactive oxygen species (ROS) production from cortical neurons through activation of NADPH oxidase. ROS derived from NADPH oxidase led to activation of extracellular signal‐regulated kinase 1/2, phosphorylation of cytosolic phospholipase A₂α (cPLA₂α), and arachidonic acid (AA) release. In addition, Aβ_1–42‐induced AA release was inhibited by d(−)‐2‐amino‐5‐phosphonopentanoic acid and memantine, two different NMDA receptor antagonists, suggesting action of Aβ through the NMDA receptor. Besides serving as a precursor for eicosanoids, AA is also regarded as a retrograde messenger and plays a role in modulating synaptic plasticity. Other phospholipase A₂ products such as lysophospholipids can perturb membrane phospholipids. These results suggest an oxidative‐degradative mechanism for oligomeric Aβ_1–42 to induce ROS production and stimulate AA release through the NMDA receptors. This novel mechanism may contribute to the oxidative stress hypothesis and synaptic failure that underline the pathogenesis of Alzheimer’s disease.

Resistance exercise is a popular form of conditioning for numerous sport disciplines, and recently different modes of strength training are being evaluated for health benefits. Resistance exercise differs significantly in nature, and several variables determine the direction and range of adaptive changes that occur in the muscular and skeletal system of the body. Some modes of resistance training can also be effective in stimulating the cardiovascular system. These variables include exercise selection (general, specific, single or multi joint, dynamic, explosive), type of resistance (free weights, variable resistance, isokinetics), order of exercise (upper and lower body or push and pull exercises), and most of all the training load which includes intensity expressed as % of 1RM, number of repetitions, number of sets and the rest interval between sets. Manipulating these variables allows for specific adaptive changes which may include gains in muscle mass, muscle strength or muscle endurance. It has been well established that during resistance exercise fatigue occurs, regardless of the volume and intensity of work applied. The peripheral mechanisms of fatigue have been studied and explained in more detail than those related to the CNS. This review is an attempt to bring together the latest knowledge regarding fatigue, both peripheral and central, during resistance exercise. The authors of this review concentrated on physiological and biochemical mechanisms underlying fatigue in exercises performed with maximal intensity, as well as those performed to exhaustion with numerous repetitions and submaximal load.

Excessive production of Aβ (amyloid β-peptide) has been shown to play an important role in the pathogenesis of AD (Alzheimer's disease). Although not yet well u...