To date (2013), we have witnessed over 100 years of research on Alzheimer’s disease (AD). In the past century, this gave new and deep insights into its pathophysiology. However, no new treatment with an innovative mode of action has found its way to the patients since the first targeted therapies with cholinergic drugs like Tacrin. So far A-beta and related targets have shown negative results in pivotal Phase III studies, after showing promising trends in Phase II. Thus the question arises as to whether A-beta is the wrong target for disease-modifying treatments, or whether other substantial changes to clinical development plans need to be made, e.g. including patients at risk of developing AD instead of those already experiencing symptoms. Alternative targets and study design options like enrichment strategies, however, do not evolve as an easy alternative solution.

Hinter körperlichen Störungen verbirgt sich im Alter oft eine Depression. Wichtig für Betroffene und ihre Angehörigen ist, dass dies frühzeitig erkannt und aktiv angegangen wird - mit der richtigen Hilfe und sinnvollen Maßnahmen zur Selbsthilfe. Das Buch bietet alles, was man wissen muss, fachkundig und lebensnah erklärt vom Leiter des Freiburger Zentrums für Geriatrie und Gerontologie. Mit Selbsttest und 10-Punkte-Präventionsprogramm.

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Abstract: Background Neuroinflammation is a key factor of Alzheimer's disease (AD) and other neurodegenerative conditions. Microglia are the resident mononuclear immune cells of the central nervous system (CNS). They play an essential role in the maintenance of homeostasis and responses to neuroinflammation. Ginkgo biloba extract EGb 761 is one of the most commonly used natural medicines owing to its established efficacy and remarkable biological activities especially in respect to CNS diseases. However, only few studies have addressed the effects and mechanisms of Ginkgo biloba extract in microglia activation. Methods We measured the production of pro-inflammatory mediators and cytokines by ELISA and analyzed gene expressions by qRT-PCR and Western Blot in LPS treated cultured primary rat microglia. Results The Ginkgo biloba extract EGb 761 significantly inhibited the release of prostaglandin E2 (PGE2) and differentially regulated the levels of pro-inflammatory cytokines. The inhibition of LPS-induced PGE2 release in primary microglia was partially dependent on reduced protein synthesis of mPGES-1 and the reduction in the activation of cytosolic phospholipase A2 (cPLA2) without altering COX-2 enzymatic activity, inhibitor of kappa B alpha (IkappaBalpha) degradation, and the activation of multiple mitogen activated protein kinases (MAPKs). Altogether, we showed that EGb 761 reduces neuro-inflammatory activation in primary microglial cells by targeting PGE2 release and cytokines. Conclusion Ginkgo biloba extract EGb 761 displayed anti-neuroinflammatory activity in LPS-activated primary microglia cells. EGb 761 was able to reduce neuroinflammatory activation by targeting the COX/PGE2 pathway. This effect might contribute to the established clinical cognitive efficacy in Alzheimer's disease, vascular and mixed dementia

Abstract: Introduction Subjective cognitive decline (SCD) and depressive symptoms (DS) frequently co-occur prior to dementia. However, the temporal sequence of their emergence and their combined prognostic value for cognitive decline and dementia is unclear. Methods Temporal relationships of SCD, DS and memory decline were examined by latent difference score modeling in a high-aged, population-based cohort (N = 3217) and validated using Cox-regression of dementia-conversion. In 334 cognitively unimpaired SCD-patients from memory-clinics, we examined the association of DS with cognitive decline and with cerebrospinal fluid (CSF) Alzheimer's disease (AD) biomarkers. Results In the population-based cohort, SCD preceded DS. High DS were associated with increased risk of dementia conversion in individuals with SCD. In SCD-patients from memory-clinics, high DS were associated with greater cognitive decline. CSF Aß42 predicted increasing DS. Discussion SCD typically precedes DS in the evolution to dementia. SCD-patients from memory-clinics with DS may constitute a high-risk group for cognitive decline. Highlights Subjective cognitive decline (SCD) precedes depressive symptoms (DS) as memory declines. Emerging or persistent DS after SCD reports predict dementia. In SCD patients, more amyloid pathology relates to increasing DS. SCD patients with DS are at high risk for symptomatic progression