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.

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The elderly population is growing worldwide, with important health and socioeconomic implications. Clinical and experimental studies on aging have uncovered numerous changes in the brain, such as decreased neurogenesis, increased synaptic defects, greater metabolic stress, and enhanced inflammation. These changes are associated with cognitive decline and neurobehavioral deficits. Although aging is not a disease, it is a significant risk factor for functional worsening, affective impairment, disease exaggeration, dementia, and general disease susceptibility. Conversely, life events related to mental stress and trauma can also lead to accelerated age-associated disorders and dementia. Here, we review human studies and studies on mice and rats, such as those modeling human neurodegenerative diseases, that have helped elucidate (1) the dynamics and mechanisms underlying the biological and pathological aging of the main projecting systems in the brain (glutamatergic, cholinergic, and dopaminergic) and (2) the effect of defective glutamatergic, cholinergic, and dopaminergic projection on disabilities associated with aging and neurodegenerative disorders, such as Alzheimer’s and Parkinson’s diseases. Detailed knowledge of the mechanisms of age-related diseases can be an important element in the development of effective ways of treatment. In this context, we briefly analyze which adverse changes associated with neurodegenerative diseases in the cholinergic, glutaminergic and dopaminergic systems could be targeted by therapeutic strategies developed as a result of our better understanding of these damaging mechanisms.

Wingate test is short anaerobic exercise, performed with maximal power, whereas aerobic exercise at 85% maximal heart rate (HR(max)) may be performed for long period. Sustained HR elevations and changes in autonomic activity indices have been observed after latter kind of exercise. Several studies reported reduction in mean interval between consecutive R peaks in ECG (RRI) 1 h after Wingate test; however, underlying changes in autonomic activity remain elusive. In eight young males, RRI and heart rate variability (HRV) were measured daily over two 5-day trials. Subjects exercised on third day of each trial, measurements were taken 1 h after (i) two consecutive 30-s bouts of Wingate tests or (ii) after a 30-min exercise at 85% HR(max), with subjects in supine rest and breathing either spontaneously or at controlled rates of 6 and 15 breaths / min. RRI was significantly shorter after Wingate and submaximal exercise, reduction of high- and low-frequency components of HRV attained reliability only after Wingate tests. This pattern remained preserved for three modes of breathing: spontaneous, 6 and 15 breaths /min. After 24 and 48 h, no exercise effects were traceable. We hypothesize that (i) anaerobic exertion is followed by sustained inhibition of vagal activity, (ii) parasympathetic system plays dominant role in mediating suppression of high- and low-HRV frequency components during postexercise recovery, (iii) degree of alteration of autonomic activity caused by anaerobic and strenuous aerobic exercise may be similar and (iv) normalization of vagal activity precedes normalization of sympathetic cardiac nerves activity during final stage of postexercise recovery.

Although the mechanisms of toxic activity of tau are not fully recognized, it is supposed that the tau toxicity is related rather not to insoluble tau aggregates but to its intermediate forms. It seems that neurofibrillar tangles (NFTs) themselves, despite being composed of toxic tau, are probably neither necessary nor sufficient for tau-induced neuronal dysfunction and toxicity. Tau oligomers (TauOs) formed during the early stages of tau aggregation are the pathological forms that play a key role in eliciting the loss of neurons and behavioral impairments in several neurodegenerative disorders called tauopathies. They can be found in tauopathic diseases, the most common of which is Alzheimer’s disease (AD). Evidence of co-occurrence of b-amyloid, α-synuclein, and tau into their most toxic forms, i.e., oligomers, suggests that these species interact and influence each other’s aggregation in several tauopathies. The mechanism responsible for oligomeric tau neurotoxicity is a subject of intensive investigation. In this review, we summarize the most recent literature on the damaging effect of TauOs on the stability of the genome and the function of the nucleus, energy production and mitochondrial function, cell signaling and synaptic plasticity, the microtubule assembly, neuronal cytoskeleton and axonal transport, and the effectiveness of the protein degradation system.

Parkinson's disease (PD) is manifested by progressive motor, autonomic, and cognitive disturbances. Dopamine (DA) synthesizing neurons in the substantia nigra (SN) degenerate, causing a decline in DA level in the striatum that leads to the characteristic movement disorders. A disease-modifying therapy to arrest PD progression remains unattainable with current pharmacotherapies, most of which cause severe side effects and lose their efficacy with time. For this reason, there is a need to seek new therapies supporting the pharmacological treatment of PD. Motor therapy is recommended for pharmacologically treated PD patients as it alleviates the symptoms. Molecular mechanisms behind the beneficial effects of motor therapy are unknown, nor is it known whether such therapy may be neuroprotective in PD patients. Due to obvious limitations, human studies are unlikely to answer these questions; therefore, the use of animal models of PD seems indispensable. Motor therapy in animal models of PD characterized by the loss of dopaminergic neurons has neuroprotective and neuroregenerative effects, and the completeness of neuronal protection may depend on (i) degree of neuronal loss, (ii) duration and intensity of exercise, and (iii) time elapsed between insult and commencing of training. As the physical activity is neuroprotective for dopaminergic neurons, the question arises what is the mechanism of this protective action. A current hypothesis assumes a central role of neurotrophic factors in the neuroprotection of dopaminergic neurons, even though it is still not clear whether increased DA level in the nigrostriatal axis results from neurogenesis of dopaminergic neurons in the SN, recovery of the phenotype of dopaminergic neurons, increased sprouting of the residual dopaminergic axons in the striatum, or generation of local striatal neurons from inhibitory interneurons. In the present review, we discuss studies describing the influence of physical exercise on the PD-like changes manifested in animal models of the disease and focus our interest on the current state of knowledge on the mechanism of neuroprotection induced by physical activity as a supportive therapy in PD.

The aim of this paper is the presentation of recent advancements in impedance cardiography regarding methodical approach, applied equipment and clinical or research implementations. The review is limited to the papers which were published over last 17 months (dated 2011 and 2012) in well recognised scientific journals. (Cardiol J 2012; 19, 5: 550-556)

The aim of the study was to compare stroke volume (SV), ejection time (ET) and pre-ejection period (PEP) measurements obtained using a central haemodynamics ambulatory monitoring device based on impedance cardiography (ICG), in supine and tilted positions (60 degrees), with pulsed Doppler echocardiography as a non-invasive reference method. The Holter-type ICG device was used for off-line, beat-to-beat, automatic determination of SV, ET and PEP. ICG data were compared with those obtained simultaneously using pulsed Doppler echocardiography in the ascending aorta from a suprasternal projection, 1 min before and 10 min after tilting. The tests were performed in 13 young, healthy subjects (six men and seven women, aged 23-33 years). Linear regression between the measured values obtained for all subjects was described by the following formulas: SVicg= 13.9 + 0.813 x SVecho (r = 0.857, SEE = 9.03, n = 496), ETicg = 16.8 + 0.987 x ETecho (r = 0.841, SEE=21.3, n = 496), PEPicg= 22.8 + 0.890 x PEPecho (r = 0.727, SEE = 14.6, n = 496). The data showed that ambulatory impedance cardiography gives useful absolute values of SV and systolic time intervals measured in supine and tilted positions.