Relationship between dystrophic neurites and plaques

Inspection of the AD brain reveals innumerable neuropil threads, dystrophic and morphologically bizarre axons and dendritic profiles, and several subtypes of senile plaques. The most prominent plaque is surrounded by tau-immunopositive swollen, dystrophic neurites (frequently referred to as a neuritic plaque). Even "normal" appearing neurites often take bizarre geometries and trajectories, curving around plaques and losing the rigid, straight appearance normally characteristic of dendrites and axons (Fig. 1).

Two alternative hypotheses have been suggested to account for the close relationship between dystrophic axons and dendrites and amyloid deposits. Goldstein and his

Fig. 1. A three-dimensional reconstruction of a plaque and a nearby neurite (filled with green fluorescent protein) from a Tg2576 mouse. This image, taken with a multiphoton microscope in a living mouse, illustrates the irregular surface and large surface area of a plaque and the dysmorphic nature of surrounding neurites. Note how the neurite courses around the plaque

Fig. 1. A three-dimensional reconstruction of a plaque and a nearby neurite (filled with green fluorescent protein) from a Tg2576 mouse. This image, taken with a multiphoton microscope in a living mouse, illustrates the irregular surface and large surface area of a plaque and the dysmorphic nature of surrounding neurites. Note how the neurite courses around the plaque colleagues (Stokin et al. 2005) hypothesize that axonal dystrophies precede and lead to senile plaques, and that axonal transport defects influence plaque deposition and lead to neural dysfunction. By contrast, we observe that axonal dystrophies resolve after application of anti-Aß antibodies, suggesting that they are secondary to Aß (Brendza et al. 2005). These observations lead to the possibility that axonal transport defects lead to axonal dystrophies and elevated Aß production leading to plaque formation, and/or plaques (or locally high Aß levels) lead to local alterations in axons, disrupting axonal transport. If so, this provides a unifying hypothesis for Aß-induced alterations in neuronal structure and function.

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