Tangles destroy a vital cell transport system made of proteins. In healthy areas, the transport system is organized in orderly parallel strands. Nutrients and other materials needed by neurons travel on these tracks. A protein called tau helps the tracks stay straight. In areas where tangles are forming, tau collapses into twisted strands called tangles. The tracks cannot stay straight and nutrients and other materials cannot reach the neurons. These cells eventually die due to a lack of nutrients (Alzheimer’s Disease & Dementia). Tau is the protein involved in tangles in the brain and tau aggregation inhibitors and tau vaccines are being researched for future treatment for people with Alzheimer’s. Hopefully these drugs will stop tau from forming
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The 4 drugs so far are donepezil, galantamine, memantine and rivastigmine. Donepezil and memantine may be used in combination to treat Alzheimer’s (Alzheimer’s Disease & Dementia). Alzheimer’s destroys synapses and kills neurons. Drugs for Alzheimer’s support the communication process of neurons by helping maintain the synapse and also tries to keep neurons from dying. Cholinesterase inhibitors slow down the process that breaks down the neurotransmitter acetylcholine. Donepezil, galantamine, and rivastigmine are cholinesterase inhibitors. Memantine works differently and is called an N-methyl-D-aspartate receptor antagonist. This regulates the activity of glutamate which is an important neurotransmitter in the brain involved in learning and memory (Alzheimer’s Disease & Dementia). Memantine blocks glutamate from binding to its receptor on the neuron. Binding of glutamate permits calcium to enter the cell. In Alzheimer’s patients, however, excess glutamate can be released from damaged cells, leading to chronic overexposure to calcium, which can speed up cell damage (Alzheimer’s Disease & Dementia). One problem with treatment for Alzheimer’s is because of something called the blood-brain barrier. The blood-brain barrier is a protective barrier that only allows certain substances into the brain. This makes it hard to get medications to the brain that may help in treatment for diseases like Alzheimer’s (Sherwood). …show more content…
One idea is to target plaques in the brain. Scientists want to target plaques by possibly recruiting the immune system. The idea is to stop beta-amyloid from clumping into plaques and also clear beta-amyloid from the brain. Research is being done with a monoclonal antibody called solanezumab and so far it seems to be effective. It seemed to be more effective when it was given earlier in the course of the disease like patients with mild Alzheimer’s (Alzheimer’s Treatments: What’s on the Horizon?). Drugs called beta-secretase and gamma-secretase inhibitors are working toward stopping the production of beta-amyloid as well (Alzheimer’s Treatments: What’s on the Horizon?). Some studies are looking at other proteins associated with beta-amyloid, rather than treating the beta-amyloid proteins directly. Beta-amyloid interacts with another protein called Fyn. When together, Fyn causes destruction of synapses in the brain. Right now research is being done to stop the action of Fyn. In studies with mice, Fyn stopped destroying synapses and some synapses even started work again and there was a reversal of memory
The 4 drugs so far are donepezil, galantamine, memantine and rivastigmine. Donepezil and memantine may be used in combination to treat Alzheimer’s (Alzheimer’s Disease & Dementia). Alzheimer’s destroys synapses and kills neurons. Drugs for Alzheimer’s support the communication process of neurons by helping maintain the synapse and also tries to keep neurons from dying. Cholinesterase inhibitors slow down the process that breaks down the neurotransmitter acetylcholine. Donepezil, galantamine, and rivastigmine are cholinesterase inhibitors. Memantine works differently and is called an N-methyl-D-aspartate receptor antagonist. This regulates the activity of glutamate which is an important neurotransmitter in the brain involved in learning and memory (Alzheimer’s Disease & Dementia). Memantine blocks glutamate from binding to its receptor on the neuron. Binding of glutamate permits calcium to enter the cell. In Alzheimer’s patients, however, excess glutamate can be released from damaged cells, leading to chronic overexposure to calcium, which can speed up cell damage (Alzheimer’s Disease & Dementia). One problem with treatment for Alzheimer’s is because of something called the blood-brain barrier. The blood-brain barrier is a protective barrier that only allows certain substances into the brain. This makes it hard to get medications to the brain that may help in treatment for diseases like Alzheimer’s (Sherwood). …show more content…
One idea is to target plaques in the brain. Scientists want to target plaques by possibly recruiting the immune system. The idea is to stop beta-amyloid from clumping into plaques and also clear beta-amyloid from the brain. Research is being done with a monoclonal antibody called solanezumab and so far it seems to be effective. It seemed to be more effective when it was given earlier in the course of the disease like patients with mild Alzheimer’s (Alzheimer’s Treatments: What’s on the Horizon?). Drugs called beta-secretase and gamma-secretase inhibitors are working toward stopping the production of beta-amyloid as well (Alzheimer’s Treatments: What’s on the Horizon?). Some studies are looking at other proteins associated with beta-amyloid, rather than treating the beta-amyloid proteins directly. Beta-amyloid interacts with another protein called Fyn. When together, Fyn causes destruction of synapses in the brain. Right now research is being done to stop the action of Fyn. In studies with mice, Fyn stopped destroying synapses and some synapses even started work again and there was a reversal of memory