© 2008 Elsevier Ltd. Alzheimer’s disease (AD), the most prevalent neurodegenerative disorder, causes progressive cognitive decline and degeneration of synapses and neurons. Some neurological impairments in AD may reflect reversible network dysfunction rather than loss of neurons. Biochemical and genetic studies have identified several molecules that may play a causal role in the pathogenesis of AD. We will review how these molecules impair memory. Many molecules that are important for synaptic plasticity are altered in AD, including receptors, channels, kinases, and neuromodulators. We will discuss how these alterations could contribute to deficits in synaptic plasticity and memory and review promising entry points for therapeutic interventions.