Alzheimer’s disease affects more than 15 million individuals worldwide from mild to severe. (Lilienfeld, 2006). It is a progressive and irreversible disease that leads to full dependency on a caretaker due to the decline in cognitive function and ability to perform daily tasks (Richarz, Gaudig, Rettig, & Schauble, 2014). Alzheimer’s disease is the most common form of dementia and normally occurs within individuals 60 years of age or older (Lilienfeld, 2006). Every twenty years the number of individuals affected by dementia is expected to double. This estimates 65.7 million people suffering from dementia in 2030 and 115.4 million in 2050 (Richarz et al., 2014). As individuals age, a patient’s likeness to obtain this condition rapidly increases.
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Inhibiting AChE increases the availability of ACh in the synaptic cleft, which is a neurotransmitter involved in the production of cholinergic neurons. By inhibiting the breakdown of ACh, Galantamine binds competitive and reversibly to AChE especially in the frontal cortex and hippocampus portions of the brain. These two regions are the most affected portions of the brain affected in those with Alzheimer’s disease. The numbers of nAChRs directly affect or modulate cholinergic neurons and other neurotransmitters. This indicates that there may be a direct relationship between the number of nAChRs in other parts of the brain to regulate mood and psychological imbalance. Low amounts of neurotransmitters and synaptic connections are present in patients with Alzheimer’s disease. This leads to a cholinergic deficient that can affect cognition, learning, and memory, and behavior. Deficits in learning and memory are linked to decreased amounts of glutamate, and reduced serotonin (5-HT) amounts are linked to emotional disturbances including anxiety or depression. In the brains of those with Alzheimer’s disease the number of nAChRs tend to be reduced. Impairments in cognition are due to the blockage of nAChRs. Galantamine binds allosterically (secondarily) to a specific protein subunit of the nAChRs to which ACh binds. Galantamine potentiates stronger neurotransmissions by making nAChRs more sensitive to
Inhibiting AChE increases the availability of ACh in the synaptic cleft, which is a neurotransmitter involved in the production of cholinergic neurons. By inhibiting the breakdown of ACh, Galantamine binds competitive and reversibly to AChE especially in the frontal cortex and hippocampus portions of the brain. These two regions are the most affected portions of the brain affected in those with Alzheimer’s disease. The numbers of nAChRs directly affect or modulate cholinergic neurons and other neurotransmitters. This indicates that there may be a direct relationship between the number of nAChRs in other parts of the brain to regulate mood and psychological imbalance. Low amounts of neurotransmitters and synaptic connections are present in patients with Alzheimer’s disease. This leads to a cholinergic deficient that can affect cognition, learning, and memory, and behavior. Deficits in learning and memory are linked to decreased amounts of glutamate, and reduced serotonin (5-HT) amounts are linked to emotional disturbances including anxiety or depression. In the brains of those with Alzheimer’s disease the number of nAChRs tend to be reduced. Impairments in cognition are due to the blockage of nAChRs. Galantamine binds allosterically (secondarily) to a specific protein subunit of the nAChRs to which ACh binds. Galantamine potentiates stronger neurotransmissions by making nAChRs more sensitive to