QUESTION: Short essay...short essay. Based of the two falculty research summarys

Question

QUESTION: Short essay...short essay. Based of the two falculty research summarys I posted that I'm interested in, "what research topics you would like to pursue for your masters research project and why?." I also personally want to become a PA in oncology in a few years.

1) RESEARCH SUMMARY

Neuronal Blockages and Alzheimer’s: How traffic moves along the neuronal highways in the brain.

Within axons vital cargoes must be transported over great distances along microtubule tracks to maintain cell viability. In neuronal cells, many proteins function in sending and receiving messages, cell repair, and cell protection. My interest is to elucidate if degeneration of neurons in two neurodegenerative diseases (Alzheimer’s disease or Huntington’s/other polyQ diseases), is related to a defect in this long distance transport system and what mechanisms facilitate the normal transport of APP and huntingtin.

2)

RESEARCH SUMMARY

The Xu-Friedman lab studies the mechanisms and functions of synaptic plasticity, focussing on auditory nerve synapses in the mouse cochlear nucleus as a model system. The lab investigates both activity- and neuromodulator-dependent plasticities, using electrophysiology and calcium imaging in brain slices. In addition, the functional effects of plasticity are being studied by recording from auditory nerve and cochlear nucleus in vivo

Explanation / Answer

(1) Alzheimer's disease or AD is a progressive, degenerative brain disease that destroys a person's ability to think, reason or perceive information. It develops as a result of loss of neurons and synapses and the brains. It can be studied in two ways.

DOMINANTLY INHERITED FORMS OF AD:
This is caused as a result of a missense mutation in the amyloid precursor protein (APP) or presenilin genes 1 or 2, causing increase in amyloid beta 42 production throughout life. This leads to the accumulation and oligomerization of this amyloid beta 42 in the limbic and association cortices affecting the synaptic efficacy of the neurons. The gradual deposition of amyloid beta 42 oligomers starts diffusing as plaques and causes microglial and astrocytic activation and attendant inflammatory responses. There is altered neuronal ionic homeostasis and oxidative injury, altered neuronal kinase and phosphatase activity (tangles) leading to widespread neurona/synaptic dysfunction and selective loss with attendant neurotransmitter deficiency and dementia.

NON-DOMINANT/SPORADIC FORMS OF AD:
In the sporadic form, there is a ApoE4 inheritance or faulty amyloid beta degradation failure causing a failure in clearing the amyloid beta, leading to the accumulation of amyloid beta 42 levels.

(2) The cell-type specific short-term plasticity in the auditory nerve synapses control the feed-forward inhibition in the dorsal cochlear nucleus. The short-term synaptic plasticity of auditory nerve-evokes the disynaptic inhibition onto fusiform cells, which exhibits facilitation when activated directly by stimulating inhibitory inputs onto the fusiform cells.

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