Titlebook: Ageing and Dementia; Current and Future C Kurt A. Jellinger,Reinhold Schmidt,Manfred Windisc Conference proceedings 2002 Springer-Verlag Wi

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,Measuring cognition in advanced Alzheimer’s disease for clinical trials,te Examination (MMSE) and the AD Assessment Scale (ADAS). With the exception of clinical rating scales, however, there are only a few objective measures of cognition for tracking progression in advanced AD. Given renewed interest in potential therapies for advanced AD, objective measures of cognitio

CRP743

,Current drugs and future hopes in the treatment of Alzheimer’s disease,disease progression remains still unclear. New cholinesterase inhibitors should provide an additional neuroprotective activity, because only substances which stop neuronal death can influence disease progression. New treatment strategies are focusing on amyloid processing, preventing the occurrence

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Development of human antibody fragments directed towards synaptic acetylcholinesterase using a semiticholinesterases promote alternative splicing changing the composition of brain AChE variants. To study this phenomenon we developed monoclonal antibodies to acetylcholinesterase synaptic peptide (ASP), a synthetic peptide with the C-terminal sequence unique to the human synaptic variant AChE-S. Sc

dictator

,Long-term stabilizing effect of cholinesterase inhibitors in the therapy of Alzheimer’ disease,ed for the first time in USA and Europe. All three compounds are cholinesterase inhibitors (ChEI). The major therapeutic effect of ChEI on AD patients is to maintain cognitive function at a stable level during a 6 months to one year period of treatment as compared to placebo. Additional drug effects

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,Nicotinic receptor modulation: Advantages for successful Alzheimer’s disease therapy,rs (nAChRs). In this report, these two effects are shown to be dependent upon each other using a realistic computer model of the cholinergic synaptic cleft. The model is based upon realistic estimates of the anatomy of a neuronal synapse, the kinetic states of pre-and postsynaptic nAChRs, and the ac

Apraxia

0303-6995 nced our knowledge about ageing processes of the human brain, its sequelae, diagnostic, and therapeutic possibilities and limits. In addition to Alzheimer‘s disease and other degenerative dementias, the impact of cerebrovascular lesions and their risk factors in the pathogenesis of cognitive disorde

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