[Introduction - Mental health has crucial role in our life. Cognitive changes or decline can lead to many difficulties in daily routine of older people (e.g. organization of daily activities), which can, consequently, influence their well-being. Therefore it is an important question, which cognitive abilities are affected by age-related decline. Methods - In our study we aimed to investigate the changes of cognitive abilities in healthy older adults between 61 and 85 years of age compared to the performance of younger adults. Digit span, counting span, listening span, letter fluency, semantic fluency and action fluency tests were used to assess cognitive abilities, namely working memory and executive functions. Results - The results showed that younger adults performed significantly better in all tests than older adults. Importantly, the performance of older adults was better on tests requiring less complex mental computations (e.g. digit span test) than on more complex tests where both storing and mani-pulating information was required (e.g., counting span test). We also showed that within the older age group, cognitive functions’ decline was linearly associated with increasing age. Conclusion - The present study used several, well-established neuropsychological tests to map the changes of working memory and executive functions in healthy older adults between 61 and 85 years of age compared to younger adults. Our findings can contribute to the development of prevention programs aimed at improving the quality of life of older adults and preventing age-related cognitive decline.]

[Alzheimer’s disease is the most common form of dementia in mid- and late life. The 7-10% of the population over 65 and the 50-60% of the population over 85 are affected by this disease. On the contrary of its prevalence the pathogenesis of the disease is not well defined and there is no effective neuroprotective therapeutic agent. Three predominant neuropathological features of the Alzheimer’s disease brain are intracellular neurofibrillary tangles consisting mainly of the hyperphosphorylated protein t; the extracellular amyloid deposits (neuritic plaques) consisting of amyloid b peptide; and the extensive neuronal cell loss in the hippocampus and in portions of the cerebral cortex. The possible reason of the extensive neuronal cell loss can be the mitochondrial dysfunction observed in Alzheimer’s disease. Beyond the unclarified pathogenesis the causality of these characteristic neuropathologic phenomena are still unknown. In this study we would like to deal with two actual hypotheses, with the amyloid cascade and with the mitochondrial cascade hypotheses. We try to give an overview of these two hypotheses and to depict their interrelationship.]

[This is a comprehensive paper in three parts covering history, prevalence, clinical forms, differential diagnosis, genetics, molecular pathomechanism, pathology, clinical diagnosis and treatment of frontotemporal dementia (FTD). The second part focuses on the differential diagnosis, genetics, molecular pathomechanism and pathology. The clinical diagnosis of frontotemporal dementia is based on the presence of a prominent disturbance of the executive function and of frontal lobe syndrome or a progressive aphasic syndrome without severe global cognitive impairment. Of other dementias, it is primarily Alzheimer’s disease that it should be differentiated from, but other psychiatric disorders must also be ruled out. The disease has familial and sporadic forms. Recent identification of mutations in the gene encoding the microtubule-associated tau protein in the inherited frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) has demonstrated that various tau dysfunctions can lead to neurodegeneration. Tau gene mutations have varied effects on the biology and function of the protein. This heterogeneous pathomechanism explains the wide range of clinical and neuropathological features observed in the FTDP-17. Tau and ubiquitin antibodies can be detected by sensitive immunohistochemical methods. The diagnosis of FTD should be based on neuropathological examination, and this is also the only method by which it can be definitely differentiated from other types of dementias.]

[The renin-angiotensin system (RAS) is one of the most important mechanisms regarding the pathomechanism and treatment of hyprtension. The most of the elements of the RAS are found in the nervous system too. The effect of angiotensin converting enzyme inhibitors and angiotensin receptor blockers (ARBs) is based on the inhibition of the RAS. ARBs might have a special role in the central nervous system because they do not decrease the production of angiotensin but inhibit its harmful effects mediated through the AT1 receptor while allowing the stimulation of AT2 receptors with resulting pleiotrophic actions. Hypertension is the most important risk factor for stroke and has a negative effect on cognitive functions. Antihypertensive treatment has an effect on the nervous system; in addition to the consequences of the reduced blood pressure, ARBs might provide additional advantages in stroke and dementia prevention.]

[Inclusion body myositis is the most common disabling inflammatory myopathy in the elderly. It is more frequent in men and after the age of 50 years. Inflammatory and degenerative features coexist. There is a T-cell mediated autoimmunity driven by in situ clonally expanded cytotoxic CD8-positive T-cells invading non-necrotic muscle fibres expressing MHC-I antigen. The hallmarks of degeneration are the deposition of protein aggregates and the formation of vesicles. The course of the disease is slow and the diagnosis is usually set after several years. The muscle weakness and wasting is assymetric, affecting predominantly distal muscles of the upper extremity and proximal muscles of the legs. The signs and clinical course can be characteristic, but the diagnosis is established by muscle biopsy. There is currently no evidence based effective treatment for sIBM. Prednisone, azathioprine, methotrexate, cyclosporine and IFN-β failed. Oxandrolon did not improve symptoms. Treatment with intravenous immunglobuline (IVIG) induced in some patients a transient improvement of swallowing and of muscle strenght, but the overall study results were negative. A T-cell depleting monoclonal antibody (alemtuzumab), in a small uncontrolled study slowed down disease progression for a six-month period. Repeated muscle biopsies showed the reduction of T-cells in the muscle and the suppression of some degeneration associated molecules. An effective therapeutic mean should act on both aspects of the pathomechanism, on the inflammatory and the degenerative processes as well.]