ABSTRACT
In the last years an increased interest in the electrical stimulation has consisted in the treatment of dysphagia. In the article we introduce the anatomical and physiological premises for the method. In a critical analysis the present state of art is represented, the clinical results are checked and the chances for the future are examined.
Subject(s)
Deglutition Disorders/therapy , Electric Stimulation Therapy/methods , Transcutaneous Electric Nerve Stimulation/methods , Animals , Cranial Nerves/physiopathology , Deglutition Disorders/physiopathology , Electrodes, Implanted , Electromyography , Esophageal Sphincter, Upper/innervation , Esophageal Sphincter, Upper/physiopathology , Glottis/innervation , Glottis/physiopathology , Humans , Hypopharynx/innervation , Hypopharynx/physiopathology , Motor Neurons/physiology , Nerve Fibers/physiology , Peristalsis/physiology , Pharynx/innervation , Pharynx/physiopathology , Sensory Receptor Cells/physiologyABSTRACT
Manual medicine aims at diagnosing and treating different disorders of the musculoskeletal system. It is a multidisciplinary approach with special emphasis on reversible disorders of the joints, muscles and ligaments. This treatment conception includes chirotherapy, physical therapy and drug treatment. The spine, an in particular the cervical spine, is treated primarily for joint disorders characterized by a variety of symptoms (e.g.headache, vertigo, dizziness, blurred vision). Manual medicine should be an integral part of modern clinical otolaryngology.
Subject(s)
Cervical Vertebrae/injuries , Joint Diseases/diagnosis , Joint Diseases/therapy , Manipulation, Chiropractic/methods , Palpation/methods , Spinal Diseases/diagnosis , Spinal Diseases/therapy , Cervical Vertebrae/physiopathology , Humans , Joint Diseases/physiopathology , Manipulation, Spinal/methods , Spinal Diseases/physiopathologyABSTRACT
An increasing number of proteins are implicated in apoptosis and several of them have been shown to be altered in Alzheimer's disease (AD) brain. Because of this apoptosis is thought to be the underlying mechanism of neuronal cell loss in AD. To further substantiate this hypothesis we investigated the expression of a recently identified apoptosis related proteins and other apoptosis regulators in frontal cortex and cerebellum of AD by Western blot and enzyme-linked immunsorbent assay technique. Quantitative analysis revealed unaltered levels of Bax and RAIDD (Receptor interacting protein associated ICH-1 (caspase-2)/CED-3 (Caenorhabditis elegans death protease-3)-homologous protein with death domain) in both regions. ZIP (Zipper interacting protein) kinase, Bim/BOD (Bcl-2 interacting mediator of cell death/Bcl-2 related ovarian death gene) and p21 were significantly increased only in AD frontal cortex (P < 0.05, in all cases). Cerebellar Bcl-2 levels were significantly increased in AD (P < 0.01) while in AD frontal cortex, although the levels tended to increase did not reach significance level. The results indicate that apoptosis indeed account for the neuronal loss in AD. However, it does not seem to involve Bax and RAIDD.
Subject(s)
Alzheimer Disease/metabolism , Apoptosis/physiology , Cerebellum/metabolism , Frontal Lobe/metabolism , Membrane Proteins , Nerve Degeneration/metabolism , Nerve Tissue Proteins/metabolism , Neurons/metabolism , Aged , Alzheimer Disease/pathology , Alzheimer Disease/physiopathology , Apoptosis Regulatory Proteins , Bcl-2-Like Protein 11 , Blotting, Western , Calcium-Calmodulin-Dependent Protein Kinases , Carrier Proteins/metabolism , Cerebellum/pathology , Cerebellum/physiopathology , Cyclin-Dependent Kinase Inhibitor p21 , Cyclins/metabolism , Death-Associated Protein Kinases , Female , Frontal Lobe/pathology , Frontal Lobe/physiopathology , Humans , Male , Middle Aged , Nerve Degeneration/pathology , Nerve Degeneration/physiopathology , Neurons/pathology , Protein Serine-Threonine Kinases/metabolism , Proto-Oncogene Proteins/metabolism , Proto-Oncogene Proteins c-bcl-2/metabolism , bcl-2-Associated X ProteinABSTRACT
Down syndrome (DS) is a genetic disease with developmental brain abnormalities resulting in early mental retardation and precocious, age dependent Alzheimer-type neurodegeneration. Furthermore, non-cognitive symptoms may be a cardinal feature of functional decline in adults with DS. As the serotonergic system plays a well known role in integrating emotion, cognition and motor function, serotonin (5-HT) and its main metabolite, 5-hydroxyindol-3-acetic acid (5-HIAA) were investigated in post-mortem tissue samples from temporal cortex, thalamus, caudate nucleus, occipital cortex and cerebellum of adult patients with DS, Alzheimer's disease (AD) and controls by use of high performance liquid chromatography (HPLC). In DS, 5-HT was found to be age-dependent significantly decreased in caudate nucleus by 60% (DS: mean +/- SD 58.6 +/- 28.2 vs. Co: 151.7 +/- 58.4 pmol/g wet tissue weight) and in temporal cortex by about 40% (196.8 +/- 108.5 vs. 352.5 +/- 183.0 pmol/g), insignificantly reduced in the thalamus, comparable to controls in cerebellum, whereas occipital cortex showed increased levels (204.5 +/- 138.0 vs. 82.1 +/- 39.1 pmol/g). In all regions of DS samples, alterations of 5-HT were paralleled by levels of 5-HIAA, reaching significance compared to controls in thalamus and caudate nucleus. In AD, 5-HT was insignificantly reduced in temporal cortex and thalamus, unchanged in cerebellum, but significantly elevated in caudate nucleus (414.3 +/- 273.7 vs. 151.7 +/- 58.4 pmol/g) and occipital cortex (146.5 +/- 76.1 vs. 82.1 +/- 39.1 pmol/g). The results of this study confirm and extend putatively specific 5-HT dysfunction in basal ganglia (caudate nucleus) of adult DS, which is not present in AD. These findings may be relevant to the pathogenesis and treatment of cognitive and non-cognitive (behavioral) features in DS.
Subject(s)
Alzheimer Disease/metabolism , Brain/metabolism , Down Syndrome/metabolism , Serotonin/metabolism , Adult , Alzheimer Disease/pathology , Brain/pathology , Caudate Nucleus/metabolism , Cerebellum/metabolism , Chromatography, High Pressure Liquid , Female , Humans , Hydroxyindoleacetic Acid/metabolism , Male , Middle Aged , Occipital Lobe/metabolism , Reference Values , Temporal Lobe/metabolism , Thalamus/metabolismABSTRACT
Neuropathological findings of Alzheimer's disease (AD) are intracellular (neurofibrillary tangles) and extracellular (senile plaques) filamentous protein aggregates. Non-enzymatic glycation has been proposed as a primary factor in this pathogenesis, leading to increased insolubility of tau protein and beta-amyloid. The aim of our study was to test the hypothesis that increased glycoxidation, i.e. increased levels of oxidized products from non-enzymatic glycation could be found in brains of patients with AD and of aged Down syndrome (DS) subjects with abundant AD-like neuropathological lesions. Frontal cortex specimens were assayed for pentosidine (Pent) and N-epsilon-carboxymethyl-lysine (CML) by reversed phase high performance liquid chromatographical methods. Pent and CML levels in AD (n = 10; Pent, 35.5 +/- 4.84 mumol/g wet-weight tissue; CML, 135.2 +/- 5.0 mumol/g wet-weight tissue) were comparable to DS (n = 9; Pent, 36.4 +/- 3.21; CML, 133.5 +/- 4.7) and controls (n = 10; Pent, 35.2 +/- 3.55; CML, 136.9 +/- 3.3). We conclude that the results are not compatible with the concept of increased glycoxidation in AD compared to normal aging.
Subject(s)
Alzheimer Disease/metabolism , Alzheimer Disease/pathology , Aged , Aged, 80 and over , Choline O-Acetyltransferase/metabolism , Down Syndrome/metabolism , Down Syndrome/pathology , Female , Frontal Lobe/metabolism , Frontal Lobe/pathology , Glycosylation , Humans , Male , Middle Aged , Neurofibrillary Tangles/enzymology , Neurofibrillary Tangles/pathology , Oxidation-ReductionABSTRACT
Polyamines may play an important role in brain development, mature brain function and also in neurodegenerative conditions. We investigated polyamine levels in frontal cortex of human post-mortem brain samples of elderly patients with Down syndrome (DS), Alzheimer disease (AD) and normal controls by means of chromatographic separation after dansylation. Spermidine and spermine concentrations were markedly decreased in DS and AD. Polyamine levels were neither related to age and post-mortem interval nor to choline acetyltransferase activity, as indicator of neuronal loss. Our results support the idea that besides other neurotransmitter systems, endogenous polyamine levels are altered in dementing illnesses such as Alzheimer disease and Down syndrome.