Alzheimer’s disease (AD) is the most common form of dementia characterized by impaired cognitive functions associated with altered neurotransmitter levels in the brain. In AD with advancement of age, symptoms that affect memory, learning ability, language perception, and behavior start to progress. These shifts correlate with accumulations of amyloid beta plaques and neurofibrillary tangles. Such pathological changes are thought to distort synaptic neurotransmitter levels and interrupt neuron-toneuron functioning. The current drugs in AD, like donepezil, rivastigmine, etc., rely to a significant extent on ameliorated cholinergic neurotransmission and utilization of anticholinesterase inhibitors. The recent outbreaks in this disease also target neurotransmitters such as dopamine, serotonin, and their receptor signaling, rather than focusing on cholinergic neurotransmission. This concept emerges due to findings of altered neurotransmitter levels in the post mortem brains of AD patients. The current review summarizes some data underlying mechanisms targeting the role of neurotransmitters and their association with AD, as well as those related to the respective therapeutic aspects. In addition, the review describes advances in recent drugs targeting neurotransmission preclinically and clinically for their neuroprotective role in AD.