Acetylcholine (ACh) plays a crucial role in both peripheral and central nervous systems. It is synthesized by choline acetyltransferase (ChAT) from choline and acetyl-CoA, then stored in synaptic vesicles by the vesicular acetylcholine transporter (VAChT). ACh is released into the synaptic cleft upon neuronal depolarization, where it binds to muscarinic and nicotinic receptors, leading to either stimulatory or inhibitory responses. The enzyme acetylcholinesterase (AChE) rapidly hydrolyzes ACh, releasing acetate and choline, which are recycled back into the presynaptic neuron via the high-affinity choline transporter (CHT1). Cholinergic neurons, particularly those in the basal forebrain including the nucleus basalis of Meynert, are severely lost in Alzheimer's disease (AD). This loss contributes to memory and attention deficits in AD patients. The cholinergic system is involved in critical physiological processes such as attention, learning, memory, stress response, wakefulness, and sleep. Synaptic loss is the principal correlate of disease progression in AD, and drugs targeting the cholinergic system are promising for treating AD. Cholinergic neurotransmission involves the synthesis, storage, and release of ACh, as well as its inactivation by AChE. The cholinergic system also regulates sleep cycles and sensory information processing. ACh is involved in various aspects of memory, including acquisition, encoding, consolidation, reconsolidation, extinction, and retrieval. The cholinergic system is also involved in stress responses and modulates the hypothalamic-pituitary-adrenal (HPA) axis. In AD, the loss of cholinergic neurons and the subsequent impairment in cholinergic neurotransmission contribute to cognitive decline. The cholinergic system is also involved in the pathogenesis of AD, with evidence suggesting that AChE may interact with β-amyloid peptides and promote amyloid fibril formation. Cholinesterase inhibitors such as donepezil, galantamine, and rivastigmine are used to treat AD by increasing ACh levels in the synaptic cleft and improving cognitive symptoms. Other drugs targeting the cholinergic system, such as M1 muscarinic receptor agonists and allosteric modulators, are being investigated for their potential to treat AD. These drugs may help reduce Aβ production, increase trophic factors, and decrease glutamate excitotoxicity. Additionally, drugs that increase choline reuptake and cholinergic neuronal firing may enhance ACh synthesis and improve cognitive function in AD patients. Memantine, an NMDA receptor antagonist, is also used to treat AD by protecting cholinergic neurons from excitotoxic damage. Immunization with synthetic Aβ peptides has shown promise in reducing cognitive dysfunction and amyloid deposition in AD. However, AD immunization carries risks,Acetylcholine (ACh) plays a crucial role in both peripheral and central nervous systems. It is synthesized by choline acetyltransferase (ChAT) from choline and acetyl-CoA, then stored in synaptic vesicles by the vesicular acetylcholine transporter (VAChT). ACh is released into the synaptic cleft upon neuronal depolarization, where it binds to muscarinic and nicotinic receptors, leading to either stimulatory or inhibitory responses. The enzyme acetylcholinesterase (AChE) rapidly hydrolyzes ACh, releasing acetate and choline, which are recycled back into the presynaptic neuron via the high-affinity choline transporter (CHT1). Cholinergic neurons, particularly those in the basal forebrain including the nucleus basalis of Meynert, are severely lost in Alzheimer's disease (AD). This loss contributes to memory and attention deficits in AD patients. The cholinergic system is involved in critical physiological processes such as attention, learning, memory, stress response, wakefulness, and sleep. Synaptic loss is the principal correlate of disease progression in AD, and drugs targeting the cholinergic system are promising for treating AD. Cholinergic neurotransmission involves the synthesis, storage, and release of ACh, as well as its inactivation by AChE. The cholinergic system also regulates sleep cycles and sensory information processing. ACh is involved in various aspects of memory, including acquisition, encoding, consolidation, reconsolidation, extinction, and retrieval. The cholinergic system is also involved in stress responses and modulates the hypothalamic-pituitary-adrenal (HPA) axis. In AD, the loss of cholinergic neurons and the subsequent impairment in cholinergic neurotransmission contribute to cognitive decline. The cholinergic system is also involved in the pathogenesis of AD, with evidence suggesting that AChE may interact with β-amyloid peptides and promote amyloid fibril formation. Cholinesterase inhibitors such as donepezil, galantamine, and rivastigmine are used to treat AD by increasing ACh levels in the synaptic cleft and improving cognitive symptoms. Other drugs targeting the cholinergic system, such as M1 muscarinic receptor agonists and allosteric modulators, are being investigated for their potential to treat AD. These drugs may help reduce Aβ production, increase trophic factors, and decrease glutamate excitotoxicity. Additionally, drugs that increase choline reuptake and cholinergic neuronal firing may enhance ACh synthesis and improve cognitive function in AD patients. Memantine, an NMDA receptor antagonist, is also used to treat AD by protecting cholinergic neurons from excitotoxic damage. Immunization with synthetic Aβ peptides has shown promise in reducing cognitive dysfunction and amyloid deposition in AD. However, AD immunization carries risks,