Drug Could Derail Synapse Loss in Alzheimer’s
Link
http://neurosciencenews.com/synapse-loss-alzheimers-drug-7952/
Summary
Synapse loss is a key factor in Alzheimer’s disease that is initiated by amyloid beta peptides.There are two Wnt signalling pathways. The canonical pathway (Wnt–catenin) promotes synapse and neuronal maintenance. The non-canonical pathway (Wnt-PCP) promotes synaptic disassembly and degradation. The pathways work together to provide a balanced maintenance of synapses. In an Alzheimer disease brain the Wnt-PCP pathway is overactive and causes too much synaptic loss. The increased presence of amyloid beta protein triggers the Wnt-PCP synaptic signalling. Researchers investigated whether they could disrupt this pathway to stop the synaptic damage and spreading. The researchers treated mice with a drug called fasudil, which targets a protein called ROCK in the Wnt-PCP signalling pathway. This derais the synaptotoxic cascade of amyloid production. Fasudil shutting off the Wnt-PCP pathway, which protected synaptic spines for degradation in the amyloid beta treated neurons in vitro.
Reflection
In my Psychology of Aging class we learned about dementia and how Alzheimer's disease is the ost common form of progressive and degenerative form of dementia. The microscopic changes in the brain that cause Alzheimer's disease are rapid cell death, neurofibrillary tangles, and neurotic plaques. The rapid cell death occurs most in the hippocampus, which deals with memory. This explains why people with Alzheimer's disease have poor memory. Neurotic plaques are consisted of beta-amyloid and are surrounded by degenerated fragments of dying neurons. This fasudil drug seems to be an amazing discovery and hopefully it can help cure Alzheimer's disease one day.
http://neurosciencenews.com/synapse-loss-alzheimers-drug-7952/
Summary
Synapse loss is a key factor in Alzheimer’s disease that is initiated by amyloid beta peptides.There are two Wnt signalling pathways. The canonical pathway (Wnt–catenin) promotes synapse and neuronal maintenance. The non-canonical pathway (Wnt-PCP) promotes synaptic disassembly and degradation. The pathways work together to provide a balanced maintenance of synapses. In an Alzheimer disease brain the Wnt-PCP pathway is overactive and causes too much synaptic loss. The increased presence of amyloid beta protein triggers the Wnt-PCP synaptic signalling. Researchers investigated whether they could disrupt this pathway to stop the synaptic damage and spreading. The researchers treated mice with a drug called fasudil, which targets a protein called ROCK in the Wnt-PCP signalling pathway. This derais the synaptotoxic cascade of amyloid production. Fasudil shutting off the Wnt-PCP pathway, which protected synaptic spines for degradation in the amyloid beta treated neurons in vitro.
Reflection
In my Psychology of Aging class we learned about dementia and how Alzheimer's disease is the ost common form of progressive and degenerative form of dementia. The microscopic changes in the brain that cause Alzheimer's disease are rapid cell death, neurofibrillary tangles, and neurotic plaques. The rapid cell death occurs most in the hippocampus, which deals with memory. This explains why people with Alzheimer's disease have poor memory. Neurotic plaques are consisted of beta-amyloid and are surrounded by degenerated fragments of dying neurons. This fasudil drug seems to be an amazing discovery and hopefully it can help cure Alzheimer's disease one day.
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