Alzheimer's Dementia Essay
Alzheimer’s dementia is a neurodegenerative disease that is characterized by several brain abnormalities that are selective and only affect neurons in specific regions of the brain. This disease is characterized by a progressive decrease in neuronal activity and neuronal survival. Historically, researchers have used Magnetic Resonance Imaging (MRI) machines to scan patients with Alzheimer’s disease and the unaffected old adults and then use supercomputers to create color-coded maps which revealed the brain abnormalities. The abnormalities evident showed a degenerative sequence of Alzheimer’s disease using brain mapping. These brain maps showed a wave of gray matter loss that correlated with a progressive decline in cognitive functioning - a key feature of this disease. After comparing the scans, Alzheimer’s patients showed to have lost
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roughly 5.3% of their gray matter per year. The brain cells died even faster in the memory regions of the brain - patients lost roughly 10% of grey matter a year. Dissimilarly, unaffected old adults lost roughly 0.9% of their brain tissue every year.
In Alzheimer’s disease, certain circuits in the neocortex, the entorhinal area, hippocampus, amygdala, nucleus basalis, anterior thalamus, and several brainstem monoaminergic nuclei are at risk for losing grey matter. The dysfunction and death of neurons is associated with cytoskeletal abnormalities, in damaged brain regions. This results in a reduced amount of synaptic proteins in the brain regions within which these neurons end. These abnormalities were distributed following characteristic patterns that were specific to certain areas and even cells of the brain. When visualizing normal neurons it is evident that they contain neurofilaments. Diseased neurons show signs of neurofibrillary tangles incorporated into their neurofilaments while healthy neurons show no signs of tau. Dead neurons show solely tau proteins without any neurofilaments.
In Alzheimer’s disease, the tangles are paired helical filaments consisting of microtubule-associated protein tau.
In normal cells, the structure of the neuron is stabilized when the protein tau binds to microtubules. These neurofibrillary tangles are presumably formed through the hyperphosphorylation of tau. The key component of these mentally deteriorative plaques are neurofibrillary tangles in the cell bodies and cell projections as well as A-beta amyloid found outside the cell (extracellularly). The Alzheimer’s disease affected brain regions also contain senile plaques. These plaques have extracellular deposits of amyloid (specifically A-beta amyloid) that are surrounded by dystrophic axons.
Parkinson’s disease which is one of the most common movement disorders, was first described in 1817 and affects up to 1 million people in the United States. This well understood movement disorder is caused by the deficiency of a single neurotransmitter, dopamine. It is characterized by tremors, increased muscular tone, mask like facial expressions, flexed posture, rigidity, hypokinesia (paucity), and bradykinesia (slowness of
motion).
It is known that 80% of the dopamine in the entire brain is concentrated in the basal ganglia, which is a group of structures located at the base of the brain and involved in coordination and movement. There are two types of dopamine receptors (D1 and D2) which are located on different sets of output neurons in the stratum that allow for direct and indirect pathways. The direct pathway has the ability to provide positive feedback and the indirect pathway provides negative feedback. This occurs in a circuit between the basal ganglia and the thalamus. These pathways have opposing effects on the basal ganglia output nuclei. As a result an opposing effect in placed on the thalamic target on these nuclei. By activating the direct pathway, the thalamus is disinhibited essentially increasing thalamocortical activity. In contrast activating the indirect pathway inhibits the thalamocortical neurons even more. Subsequently, activating the direct pathway facilitates movement, while activating the indirect pathway inhibits movement. Simply put, two inhibitory synapses in the direct pathway cause net excitation and by the same logic, three inhibitory synapses in the direct pathway cause net inhibition. Parkinson’s disease causes these diverging changes in activity in the two striatopallidal projections. Additionally, basal ganglia output to the thalamus is increased in Parkinson’s patients.
roughly 5.3% of their gray matter per year. The brain cells died even faster in the memory regions of the brain - patients lost roughly 10% of grey matter a year. Dissimilarly, unaffected old adults lost roughly 0.9% of their brain tissue every year.
In Alzheimer’s disease, certain circuits in the neocortex, the entorhinal area, hippocampus, amygdala, nucleus basalis, anterior thalamus, and several brainstem monoaminergic nuclei are at risk for losing grey matter. The dysfunction and death of neurons is associated with cytoskeletal abnormalities, in damaged brain regions. This results in a reduced amount of synaptic proteins in the brain regions within which these neurons end. These abnormalities were distributed following characteristic patterns that were specific to certain areas and even cells of the brain. When visualizing normal neurons it is evident that they contain neurofilaments. Diseased neurons show signs of neurofibrillary tangles incorporated into their neurofilaments while healthy neurons show no signs of tau. Dead neurons show solely tau proteins without any neurofilaments.
In Alzheimer’s disease, the tangles are paired helical filaments consisting of microtubule-associated protein tau.
In normal cells, the structure of the neuron is stabilized when the protein tau binds to microtubules. These neurofibrillary tangles are presumably formed through the hyperphosphorylation of tau. The key component of these mentally deteriorative plaques are neurofibrillary tangles in the cell bodies and cell projections as well as A-beta amyloid found outside the cell (extracellularly). The Alzheimer’s disease affected brain regions also contain senile plaques. These plaques have extracellular deposits of amyloid (specifically A-beta amyloid) that are surrounded by dystrophic axons.
Parkinson’s disease which is one of the most common movement disorders, was first described in 1817 and affects up to 1 million people in the United States. This well understood movement disorder is caused by the deficiency of a single neurotransmitter, dopamine. It is characterized by tremors, increased muscular tone, mask like facial expressions, flexed posture, rigidity, hypokinesia (paucity), and bradykinesia (slowness of
motion).
It is known that 80% of the dopamine in the entire brain is concentrated in the basal ganglia, which is a group of structures located at the base of the brain and involved in coordination and movement. There are two types of dopamine receptors (D1 and D2) which are located on different sets of output neurons in the stratum that allow for direct and indirect pathways. The direct pathway has the ability to provide positive feedback and the indirect pathway provides negative feedback. This occurs in a circuit between the basal ganglia and the thalamus. These pathways have opposing effects on the basal ganglia output nuclei. As a result an opposing effect in placed on the thalamic target on these nuclei. By activating the direct pathway, the thalamus is disinhibited essentially increasing thalamocortical activity. In contrast activating the indirect pathway inhibits the thalamocortical neurons even more. Subsequently, activating the direct pathway facilitates movement, while activating the indirect pathway inhibits movement. Simply put, two inhibitory synapses in the direct pathway cause net excitation and by the same logic, three inhibitory synapses in the direct pathway cause net inhibition. Parkinson’s disease causes these diverging changes in activity in the two striatopallidal projections. Additionally, basal ganglia output to the thalamus is increased in Parkinson’s patients.