UNASSIGNED: @entity3986 ( @entity3986 ) are swollen and tortuous neuronal processes that are associated with extracellular depositions of amyloid b (Ab) and have been observed to contribute to synaptic alterations occurring in @entity195 . Understanding the temporal course of this axonal pathology is of high relevance to comprehend the progression of the disease over time. We performed a long-term in vivo study (up to 210  days of two-photon imaging) with two transgenic @entity19 models (dE9xGFP-M and APP-PS1xGFP-M). Interestingly, @entity3986 were formed only in a quarter of GFP-expressing axons near Ab-plaques, which indicates a selective vulnerability. @entity3986 , especially those reaching larger sizes, had long lifetimes and appeared as highly plastic structures with large variations in size and shape and axonal sprouting over time. In the case of the APP-PS1 @entity19 only, the formation of new long axonal segments in @entity3986 (re-growth phenomenon) was observed. Moreover, new @entity3986 could appear at the same point of the axon where a previous AxD had been located before disappearance (re-formation phenomenon). In addition, we observed that most @entity3986 were formed and developed during the imaging period, and numerous @entity3986 had already disappeared by the end of this time. This work is the first in vivo study analyzing quantitatively the high plasticity of the axonal pathology around Ab plaques. We hypothesized that a therapeutically early prevention of Ab plaque formation or their growth might halt disease progression and promote functional axon regeneration and the recovery of neural circuits.

High plasticity of axonal pathology in XXXX @entity19 models.

@entity19 :: ('10090', 'Species') :: ['mouse'] @entity3986 :: ('MESH:D009136', 'Disease') :: ['Axonal dystrophies', 'dystrophic axons', 'AxDs'] @entity195 :: ('MESH:D000544', 'Disease') :: ["Alzheimer's disease"]
@entity195 :: (MESH:D000544,Disease) :: ['Alzheimer's disease']
