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Functions of Presenilin1 in Glutamat...

Icahn School of Medicine at Mount Sinai.

Functions of Presenilin1 in Glutamate Release and Neuroprotection.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Functions of Presenilin1 in Glutamate Release and Neuroprotection.
Author:	Xuan, Zhao.
Description:	113 p.
Notes:	Source: Dissertation Abstracts International, Volume: 76-03(E), Section: B.
Notes:	Advisers: Nikolaos K. Robakis; Robert D. Blitzer.
Contained By:	Dissertation Abstracts International76-03B(E).
Subject:	Neurosciences.
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3641684
ISBN:	9781321281033

Functions of Presenilin1 in Glutamate Release and Neuroprotection.
Xuan, Zhao.

Functions of Presenilin1 in Glutamate Release and Neuroprotection. - 113 p.

Source: Dissertation Abstracts International, Volume: 76-03(E), Section: B.

Thesis (Ph.D.)--Icahn School of Medicine at Mount Sinai, 2014.

This item must not be sold to any third party vendors.

Alzheimer's disease (AD) is the most common form of dementia, impairing memory, cognitive function as well as basic activities of daily living at late stage. There are two types of AD, familial or early onset AD (FAD) and sporadic or late onset AD (LOAD). Mutations on presenilin (PS) 1, PS2 and amyloid precursor protein (APP) explain the etiology of FAD. Multiple risk factors including aging and presence of Apolipoprotein E (ApoE) 4 increase the change of developing LOAD. AD features massive loss of synapses and neurons, impaired cholinergic neuronal function, neuroexcitotoxicity, metabolic dysfunction as well as inflammation. FDA approved drugs to treat AD are acetylcholinesterase inhibitors, elevating the level of acetylcholine (ACh) and memantine, attenuating neuroexcitotoxicity.

ISBN: 9781321281033Subjects--Topical Terms:

211508
Neurosciences.

Functions of Presenilin1 in Glutamate Release and Neuroprotection.
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100 1 $a Xuan, Zhao. $3 708776
245 1 0 $a Functions of Presenilin1 in Glutamate Release and Neuroprotection.
300 $a 113 p.
500 $a Source: Dissertation Abstracts International, Volume: 76-03(E), Section: B.
500 $a Advisers: Nikolaos K. Robakis; Robert D. Blitzer.
502 $a Thesis (Ph.D.)--Icahn School of Medicine at Mount Sinai, 2014.
506 $a This item must not be sold to any third party vendors.
506 $a This item must not be added to any third party search indexes.
520 $a Alzheimer's disease (AD) is the most common form of dementia, impairing memory, cognitive function as well as basic activities of daily living at late stage. There are two types of AD, familial or early onset AD (FAD) and sporadic or late onset AD (LOAD). Mutations on presenilin (PS) 1, PS2 and amyloid precursor protein (APP) explain the etiology of FAD. Multiple risk factors including aging and presence of Apolipoprotein E (ApoE) 4 increase the change of developing LOAD. AD features massive loss of synapses and neurons, impaired cholinergic neuronal function, neuroexcitotoxicity, metabolic dysfunction as well as inflammation. FDA approved drugs to treat AD are acetylcholinesterase inhibitors, elevating the level of acetylcholine (ACh) and memantine, attenuating neuroexcitotoxicity.
520 $a Although it accounts for less than 5% of all AD cases, FAD displays similar pathology to LOAD and has clear etiology. Thus, FAD provides an excellent model for investigating mechanisms underlying the pathophysiology and discovering potential therapies for general AD. PS1 loss of function has been proposed to cause some FAD cases. Here we seek to further characterize the physiological roles of PS1 and investigate the mechanisms underlying synaptic dysfunction and neuronal loss due to PS1 loss of function. I focus on functions of PS1 in controlling neuroexcitotoxicity in my thesis work.
590 $a School code: 1734.
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650 4 $a Biochemistry. $3 188609
650 4 $a Cellular biology. $3 708607
650 4 $a Pathology. $3 196513
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710 2 $a Icahn School of Medicine at Mount Sinai. $b Neurosciences. $3 708777
773 0 $t Dissertation Abstracts International $g 76-03B(E).
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