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BACKGROUND Current therapy concepts for dementias are based on symptomatic treatment modalities. They do not influence the long-term course of the disease. Specific therapies that prevent the progression of neuronal cell death after outbreak of the demtia disease are currently being intensively examined in clinical studies. The present article provides a review of new developments in the diagnositics of and therapy for dementias. MATERIALS AND METHODS On the basis of the literature survey new developments in the diagnostic of and therapy for dementias are analysed. RESULTS The recently published S3 guidelines „Dementias” contain a new evaluation of diagnostics for dementias. Hereby, biomarker analysis in cerebrospinal fluid takes on an important role. In recent years efficacy analyses and meta-analyses have confirmed the utility of established symptomatic treatment modalities, in particular, of cholinesterase inhibitors and memantin, whereas therapies classied as questionable, such as GINKGO BILOBA or vitamin preparations, have largely had to be declared as inefficient on the basis of new studies. Novel therapies acting on the cause of the problem, such as, for example, β- and γ-secretase inhibitors as well as active and passive immunisation, are currently undergoing prospective randomised trials. The first of the studies to be published were negative. The results of ongoing trials are eagerly awaited.

Background: Therapeutic angiogenesis with vascular endothelial growth factor (VEGF) is a clinically promising strategy in ischemic disease. The pathophysiological consequences of enhanced vessel formation, however, are poorly understood. Methods: We here established mice overexpressing human VEGF165 under a neuron-specific NSE promoter, which exhibited an increased density of brain vessels under physiological conditions. We submitted these mice to transient focal ischemias, as induced by 90 and 30 minutes episodes of intraluminal middle cerebral artery (MCA) occlusions and examined the effects of brain-selective VEGF overexpression on ischemic injury, blood-brain barrier dysfunction, angiogenesis and regional cerebral blood flow (CBF). Results: Following 90 and 30 minutes episodes of MCA occlusions, VEGF overexpression significantly reduced neurological deficits, infarct volume, disseminate neuronal injury and caspase-3 activity. Brain swelling, on the other hand, was not influenced in VEGF-overexpressing animals, while sodium fluorescein extravasation was moderately increased, suggesting VEGF induces mild blood brain barrier leakage. In order to find out whether enhanced angiogenesis improves regional CBF in the ischemic brain, 14C-iodoantipyrine autoradiographies were performed. Autoradiographies revealed that VEGF overexpression reduces regional CBF in ischemic areas and increases blood flow values only outside the MCA territory, suggesting that enhanced angiogenesis facilitates hemodynamic steal phenomena. Conclusions: Our data suggest that brain-selective VEGF overexpression is neuroprotective via inhibition of executive cell death pathways, but worsens cerebral hemodynamics.