Effect of different exercise programs on the psychological and cognitive functions of people with Parkinson's disease

The purpose of this study was to analyze the effect of different exercise programs on the psychological and cognitive functions in patients with Parkinson's disease (PD). Forty-five patients with PD participated in the study. The participants were randomized in three intervention programs: Group-1 (n=15, cognitive-activities), Group-2 (n=15, multimodal exercise) and Group-3 (n=15, exercises for posture and gait). The clinical, psychological and cognitive functions were assessed before and after 4 months of intervention. Univariate analysis did not reveal significant interactions between groups and time (p>0.05). However, univariate analysis for time revealed differences in stress level and memory. Participants showed less physical stress (p<0.01) and overall stress (p < 0.04) and higher performance in episodic declarative memory (p < 0.001) after exercise. These findings suggest that group work with motor or non-motor activities can improve cognitive and psychological functions of patients with PD

Biomarkers for prediction and targeted prevention of Alzheimer’s and Parkinson’s diseases: evaluation of drug clinical efficacy

Neurodegenerative diseases like Parkinson’s disease (PD) and Alzheimer’s disease (AD) are considered disorders of multifactorial origin, inevitably progressive and having a long preclinical period. Therefore, the availability of biological markers or biomarkers (BMs) for early disease diagnosis will impact the management of AD and PD in several dimensions; it will 1) help to capture high-risk individuals before symptoms develop, a stage where prevention efforts might be expected to have their greatest impact; 2) provide a measure of disease progression that can be evaluated objectively, while clinical measures are much less accurate; 3) help to discriminate between true AD or PD and other causes of a similar clinical syndrome; 4) delineate pathophysiological processes responsible for the disease; 5) determine the clinical efficacy of novel, disease-modifying (neuroprotective) strategies. In the long run the availability of reliable BMs will significantly advance the research and therapeutics of AD and PD

Hidden function of neuronal nicotinic acetylcholine receptor ß2 subunits in ganglionic transmission: Comparison to ?5 and ß4 subunits

PubMedID: 15694199Neuronal nicotinic acetylcholine receptors (nAChR), which modulate fast excitatory postsynaptic potentials (f-EPSP), are located on both pre- and postganglionic sites in the autonomic nervous system (ANS). The receptor subunits ?3, ?5, ?7, ß2 and ß4 are present in autonomic ganglia in various combinations and modulate acetylcholine (ACh) transmission. In the present study, autonomic functions were systemically examined in mice lacking ß2 subunits (ß2-/-) to further understand the functional role of ß2 subunits in modulating ganglionic transmission. The results show normal autonomic functions, both under physiological conditions and in perturbed conditions, on thermoregulation, pupillary size, heart rate responses and ileal contractile reactions. This suggests that the function of ß2-containing receptors in ganglionic transmission is hidden by the predominant ß4 containing receptors and confirms previous studies which suggest that ?3?5ß4 nAChRs are sufficient for autonomic transmission. On the other hand, ß2-containing receptors have only a minor function on postsynaptic responses to ACh, but may modulate ACh release presynaptically, although there is no evidence for this. © 2004 Published by Elsevier B.V.Tel Aviv UniversityThis work was supported by the Sieratzki Chair of Neurology, Tel Aviv University, and the Miriam Turjanski de Gold Foundation

Analysis of genetic polymorphisms in acetylcholinesterase as reflected in different populations.

Acetylcholinesterase (AChE) plays a crucial physiological role in termination of impulse transmission at cholinergic synapses through rapid hydrolysis of acetylcholine. In addition, it was implicated in amyloid plaque formation, a hallmark of Alzheimer's disease (AD), and most of the drugs used in AD treatment are AChE inhibitors. Thus ACHE is an obvious candidate gene for pharmacogenetic study of AD treatment. However, AChE is a highly conserved molecule, and only a few naturally occurring genetic polymorphisms have been reported in the human gene. The goals of this study were to make a systematic effort to identify natural single nucleotide polymorphisms (SNPs) in the human ACHE gene, and to reveal their population specific architecture. To this end, the genomic coding sequences for AChE of 96 unrelated control individuals from three distinct ethnic groups, African Americans, Ashkenazi Jews and Israeli Arabs, were analyzed. Thirteen ACHE SNPs were identified, ten of which are newly described, and five of which should produce amino-acid substitutions (Arg34Gln, Gly57Arg, Glu344Gly, His353Asn and Pro592Arg). Population frequencies of 11 of the 13 SNPs were established in four different populations, African Americans, Ashkenazi Jews, Sephardic Jews and Israeli Arabs; 17 haplotypes and 5 ethno-specific alleles were identified, and a cladogram of ACHE haplotypes was constructed. Among the SNPs resulting in an amino-acid substitution, three are within the mature protein, mapping on its external surface; they are thus unlikely to affect its catalytic properties, yet could have antigenic consequences or affect putative protein-protein interactions. Furthermore, the newly identified SNPs open the door to a study of the possible association of AChE with deleterious phenotypes - such as adverse drug responses to AChE inhibitors employed in treatment of AD patients and hypersensitivity to pesticides