These transgenic models suffer axonopathy and tauopathy, respectively, but without appreciable neurodegeneration. Although data to answer this problem do not abound, we consider as major difference the observed microgliosis that is much more intense in the AAV-Tau model than in the AAV-APP mice. This is strongly reminiscent of our observations in inducible p25 mice that suffer a profound hippocampal and cortical sclerosis with pathological characteristics very similar to the AAV-Tau mice. A recent study described wild-type tau to mediate some neurodegeneration with combined microgliosis by AAV gene-transfer. Therein, degeneration of dopaminergic neurons in the substantia nigra of aged rats was also directly associated with microgliosis, lending support to our assumption that microgliosis contributes essentially to neurodegeneration. Their structural features and dynamic actions will tilt the balance to either slow death by 
progressive accumulation of aggregated, undigested or undigestible amyloid and/or protein tau, or to faster death by cell-cycle re-entry, accelerated by microglia derived proinflammatory neurotoxic factors. Moreover, the tau-species that are responsible for aggregation and neurotoxicity are proposed to differ at the molecular level. We refer here also to a most recent report on the transmission and spreading of tauopathy in transgenic mouse brain, following intracerebral injection of tau-aggregates. Those findings are relevant for the possible cell-to-cell spreading of tauopathy in brain and imply an extracellular route, which is to be defined for the cytoplasmic protein tau. Nevertheless, the time-scale of spreading was very slow and resulted in typical tauopathy with aggregates and tangles, while neuro-degeneration was minimal or absent. Thereby, that model conforms to the tauopathy as observed in the parental tau.P301S transgenic mice that have no neurodegeneration in limbic regions. In conclusion, we present in vivo experimental evidence for a major problem in tauopathies: effective modeling of pyramidal neurodegeneration that is mediated by protein tau.4R, which is responsible for the majority of human tauopathies, including all Alzheimer patients. We further delineate two major mechanisms that contribute to the rapid neurodegeneration mediated by AAVTau: attempted cell-cycle re-entry by the post-mitotic neurons, and microgliosis. We are confident that these innovative models will contribute considerably to unravel the molecular factors and mechanistic details. Importantly, the ease whereby the AAVvectors and the models can be implemented widely in researchprojects on neurodegeneration is a further strong point of this report. Development of the permanent mammalian kidney is dependent on growth and branching of the ureteric bud and its daughter branches, a process termed renal branching morphogenesis. At the onset of this process, the ureteric bud elongates Benzethonium Chloride towards and invades the metanephric mesenchyme before undergoing spatial specification into ‘ureteric stalk’ and ‘ureteric tip’ domains. Reciprocal inductive interactions between the ureteric tip and surrounding metanephric mesenchyme results in division of the ureteric tip, forming the first of a series of ureteric branches, which ultimately constitute the mature collecting duct system. Simultaneously, each ureteric bud tip induces adjacent metanephric mesenchyme cells to Ginsenoside-Ro undergo a mesenchymeepithelial transformation and form the epithelial components extending from the glomerulus to the distal tubule, a process known as nephrogenesis.