Abstract Alzheimer 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 AD pathogenesis. 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 molecular alterations, as well as cellular and network level alterations, could contribute to deficits in synaptic plasticity and memory.