It is proposed that altered dendrite length and de novo formation of new dendrite branches in cholinoceptive cells are responsible for long-term memory storage, a process enabled by the degradation of microtubule-associated protein-2. These memories are encoded as modality-specific associable representations. Accordingly, associable representations are confined to cytoarchitectonic modules of the cerebral cortex, hippocampus, and amygdala. The proposed sequence of events leading to long-term storage in cholinoceptive dendrites begins with changes in neuronal activity, then in neurotrophin release, followed by enhanced acetylcholine release, muscarinic response, calcium influx, degradation of microtubule-associated protein-2, and finally new dendrite structure. Hypothetically, each associable representation consists of altered dendrite segments from approximately 5000-15,000 cholinoceptive cells contained within one or a few module(s). Simultaneous restructuring during consolidation of long-term memory is hypothesized to result in a similar infrastructure among dendrite sets, facilitating co-activation of those dendrite sets by neurotransmitters such as acetylcholine, and conceivably enabling high energy interactions between those dendrites by phenomena such as quantum optical coherence. Based on the specific architecture proposed, it is estimated that the human telecephalon contains enough dendrites to encode 50 million associable representations in a lifetime, or put another way, to encode one new associable representation each minute. The implications that this proposal has regarding treatments for Alzheimer's disease are also discussed.