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We performed a 6-month open-label study on the use of the transdermal rivastigmine patch in clinical routine in 103 patients with Alzheimer's disease from 25 outpatient services in Austria. After baseline, safety and tolerability of the 10 cm2--rivastigmine patch was assessed at week 4, 12 and 24 in all patients. A Mini Mental State Examination was done at baseline and at week 12 and 24. Skin adherence of the patch was very good or good in 85% of study participants. Only 2.9% of patients had gastrointestinal adverse events. Local skin reactions occurred in 23% of individuals. Skin alteration were mostly mild in severity. In only 6.8% of subjects did they result in termination of treatment. At the earliest skin reactions were observed after 3 months of treatment. Cognitive functioning of patients improved comparable to the controlled trial which led to approval of the rivastigmine patch. In daily routine the safety profile of the rivastigmine patch is favourable, as is the response to treatment. Local, mostly mild skin reactions affect approximately every fifth patient, and they occur relatively late in the course of therapy. Patients and their caregivers should receive detailed information about skin reactions to omit unnecessary drop outs to treatment.

Cholinesterase inhibitors and memantine can slow the course of Alzheimer's disease. In Austria the frequency of treatment is in the upper third among countries of the EU. Yet, the majority of Alzheimer patients does not receive adequate medication. Compliance to treatment is low. Studies on cholinesterase inhibitors show that only one third and one fifth of patients adhere to medication after 3 months and 12 months, respectively. Causes for low compliance are only partly patient-related, many factors are system-inherent. Knowledge of these factors is a pre-requisite for the treating physician to improve current unfavourable situation. Present treatment strategies are symptomatic, causal disease-modifying therapies are urgently needed. Research activity in the field is high and dominated by the amyloid hypothesis. We here review the basis and recent studies on secretase-inhibitors, immunization, aggregation of Abeta, statins and PPARgamma-agonists. Research towards strategies against tau-pathology is less dominant and focuses on inhibition of kinases and increase of activity of phosphatases. Causal therapies would have great effects on a population basis even if efficacy is only moderate. A disease-modifying therapy which delays the onset of Alzheimer disease by 5 years, will probably reduce the number of patients by nearly 50% during the next 50 years.

According to the latest research the therapy of dementia includes following strategies: Above all there is a necessity for thoroughly diagnostic tests to exclude diseases which secondary induce reduced brain function. The early onset of non pharmacological treatments e.g. "brain-jogging" is essential. Pharmacological therapy with nootropics (e.g. Codergocrin, Nicergolin, Ginkgo biloba, Piracetam, Pyritinol, Naftidrofuryl) is recommended as early as possible, because they have no relevant side effects. Calcium antagonists may also be administered because of their neuroprotective properties. One pharmacological approach to enhance cholinergic functions involves inhibiting ACH-degradation by inhibiting acetylcholinesterase. Although this relatively new therapy has benefits, in some patients it has not been effective and has a potential to cause serious adverse (hepatic) events; only mild to medium severe dementias of Alzheimer's disease should be treated with this therapeutic principle. In the case of personality disorders there are psychotherapy and the administration of psychoactive drugs necessary.

In 50 healthy subjects (23 female, 27 male, aged 18-81) and 24 patients with Alzheimer's disease (AD) (11 female, 13 male, aged 58-88) DHEAS and CRT plasma levels were studied. In normal subjects there was a clear negative correlation of DHEAS to age, while no significant age correlated decrease of CRT plasma levels was found. There was a significant decrease in the DHEAS/CRT ratio in elderly controls (aged > 60) as compared to young individuals (aged < 45). Overall there was a trend to lower DHEAS/CRT ratios in AD patients compared to age matched controls out of the total group of normals (P < 0.1), there was a significant decrease of this ratio in female AD patients (P < 0.05), compared to age matched female controls, but there was none in male Alzheimers; furthermore there was a significant difference in CRT plasma levels between female AD patients and age matched female controls (P < 0.01) and between female and male AD patients (P < 0.05). Considering the antiglucocorticoid effects of DHEAS, this ratio may account for its protective effect against hippocampal degeneration caused by glucocorticoids and possibly for the higher rate of AD in females.