abeta deposition is associated with neuropil changes but not with overt neuronal loss in the human amyloid precursor protein v717f pdapp transgenic mouse the pdapp transgenic mouse overexpresses human amyloid precursor protein v717f pdapp minigene and develops agerelated cerebral amyloidbeta protein abeta deposits similar to senile plaques in alzheimers disease we find agerelated cortical and limbic abeta deposition that begins at 8 months and progresses to cover 2050 of the neuropil in cingulate cortex entorhinal cortex and hippocampus of 18monthold heterozygotic animals the regional patterns of transgene expression and amyloid deposition suggest that abeta deposits occur at the terminals of overexpressing neurons amyloid deposition is associated with dystrophic neurites and extensive gliosis however stereological analysis shows that there is no overt neuronal loss in entorhinal cortex ca1 hippocampal subfield or cingulate cortex through 18 months of age in addition there is no apparent loss of mrna encoding neuronal synaptic cytoskeletal or metabolic proteins thus widespread abeta deposition in 18monthold heterozygotic mice produces neuritic alterations and gliosis without widespread neuronal death