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	Acetylcholine and glutamate, two neurotransmitters involved in learning and memory, have been observed in various dementias and neurodegenerative diseases. Existing therapies for treating AD seek to block the enzyme that isinvolved in the degradation of acetylcholine. Glutamate is the major excitatory transmitter in the CNS, and plays an integral role in learning and memory. It is believed that abnormal glutamatergic activity may cause neuronal toxicity and impair learning. In the glutamatergic hypothesis of AD, it is proposed that abnormal glutamatergic activity results in a sustained low-level activation of the NMDA receptor. Low-level activation leads to disturbances in the natural/physiological glutamatergic neurotransmission. Chronic insult results in neuronal damage/loss in brain regions associated with learning and memory, manifested as cognitive deficits.