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. Author manuscript; available in PMC: 2008 Jul 1.
Published in final edited form as: Neuron. 2004 Sep 2;43(5):633–645. doi: 10.1016/j.neuron.2004.08.013

Figure 1. Dendritic Caspase Activation and Selective Drebrin Loss in Tg2576 Mouse and Selective Postsynaptic Marker Loss in Alzheimer’s Disease.

Figure 1

(A–C) Fractin immunoreactivity was detected in dendrites (de) and occasionally in spines (s) but not in axons (ax) in the cortex of aged Tg2576 mice. Calibration bars, 500 nm.

(D) Drebrin (Dr) in young (6–8 months) Tg(+) mice compared to old (16–18 months) Tg(+) mice in lysate from cortical membrane fractions. Values shown are percentage of young Tg(+) as the mean ± SEM. ‡‡p < 0.01 versus young Tg(+).

(E) Effect of transgene on fractin/actin ratio, drebrin (Dr), and synaptophysin (S) levels in membrane fraction of mouse cortex. Transgenic (+), n = 7–8, controls (−), n = 7–12. **p < 0.01 versus controls [Tg(−)].

(F) Drebrin (Dr), PSD-95 (PSD), and synaptophysin (S) in temporal cortex samples from AD patients (n = 10) and controls (n = 9). Values shown are percentage of control patients as the mean ± SEM. *p < 0.05, **p < 0.01 versus controls (Ctrl).

(G) Diagram illustrating the generation of fractin from cleavage of actin by caspases.