Evidences p(HGNC:RAB5A) to bp(GO:endocytosis)

Endocytic pathway up-regulation in AD stemming in part from pathological rab 5 activation generates higher levels of Ab (Mathews et al. 2002; Grbovic et al. 2003) that must be cleared in part by lysosomes.

Pathological rab5 activation, which in Down syndrome is dependent on bCTF generation (Jiang et al. 2010), can up-regulate endocytosis in a manner functionally equivalent to the elevated endocytosis associated with increased synaptic activity, which is considered a source of Ab generation (Cirrito et al. 2008).

Pathological Rab5 activation driving endocytic dysfunction in AD may negatively impact longterm potentiation (LTP) and long-term depression (LTD) aspects of synaptic plasticity closely associated with learning and memory (Kessels et al. 2009)

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