Whereas at 3 months of age APP transgenic hippocampal neurons showed no cytoskeletal abnormalities, at 11 months of age evidence of degeneration existed in all the parameters examined. Many neurons displayed dystrophic neurites, reduced dendritic arborization, and loss of spines. Most intriguing, however, were data suggestive of regenerative activity at a time-point in between – at 8 months of age, as rare dystrophic neurites became noticeable, a small increase in the number of spines and total dendritic area was observed in APP transgenic neurons in comparison to controls. Dendritic proliferation and sprouting in human AD brain have been observed by Golgi impregnation and by MAP2 and tau immunohistochemistry highlighting growth cones present both in perisomatic dendrites and in distal, dystrophic neurites. Thus, an AD transgenic model and a human diseased brain share the hallmark of cytoskeletal reorganization underlying degenerative as well as regenerative changes. Here we report an increase in the expression of Capzb2, a protein necessary for normal growth cone morphology and neurite length, specifically in the hippocampal CA1 region at mid-stage AD. This increase in Capzb2 expression could not have been aided by the astrocytic gliosis was less prominent in AD BBIII-IV brains than in control brains. Consistent with our findings are previously reported GFAP mRNA age-related increase in archi- and neo-cortex of both rats and humansand widespread astrocytic gliosis in both Alzheimer’s and normal aging cerebrum. Important for our Pazopanib molecular weight analysis was the definition of normal, “control” cases considering that the cognitive function appears to be degraded in the non-demented individuals who do exhibit AD- related neuropathological changes. We performed tau immunohistochemistry on all of the studied hippocampal blocks and considered as controls only those without any neurofibrillary tangles. The protein expression analysis of the CA1 region is supported by the data on Capzb2 mRNA expression in hippocampal CA1 neurons obtained via LCM. Several pathologic features of AD make cell population expression profiling a rational alternative to whole brain homogenates: 1) defined vulnerable neuronal populations; 2) distinct intracellular abnormalities found in some but not all of the cells; and 3) the poor understanding of the relationship between the presence of distinct extra- and intracellular abnormalities and neuronal function and survival. The importance of cell population expression profiles is in their potential to identify new rational targets for pharmacotherapeutic interventions in progressive neurodegenerative disorders such as AD. Mature brain derived neurotrophic factor or BDNF shows highaffinity binding to the neurotrophic tyrosine kinase receptor TrkB. The molecular basis for new learning is a rapid effect on synaptic transmission followed by persistent changes, such as long-term potentiation, across neuronal synapses that consolidate long-term memories.