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Association Between Large Vessel (Ar...

Simpson, Dominic,

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Association Between Large Vessel (Arterial) Dilatation and Pathological Markers of Vascular Dementia and Alzheimer's Disease /

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Association Between Large Vessel (Arterial) Dilatation and Pathological Markers of Vascular Dementia and Alzheimer's Disease // Dominic Simpson.
作者:	Simpson, Dominic,
面頁冊數:	1 electronic resource (185 pages)
附註:	Source: Dissertations Abstracts International, Volume: 86-05, Section: B.
Contained By:	Dissertations Abstracts International86-05B.
標題:	Neurosciences. -
電子資源:	https://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=31560258
ISBN:	9798342751933

Association Between Large Vessel (Arterial) Dilatation and Pathological Markers of Vascular Dementia and Alzheimer's Disease /
Simpson, Dominic,

Association Between Large Vessel (Arterial) Dilatation and Pathological Markers of Vascular Dementia and Alzheimer's Disease /Dominic Simpson. - 1 electronic resource (185 pages)

Source: Dissertations Abstracts International, Volume: 86-05, Section: B.

In my thesis, we look at the association between vascular dementia and Alzheimer's disease (AD) and how vascular changes can contribute to AD pathology. AD is the pathological presence of amyloid plaque and neurofibrillary tangles, while vascular dementia is a reduction in blood flowing to the brain due to vascular impairment. In the pathogenesis for AD and vascular changes, matrix metalloproteinases (MMPs) are gaining traction to have a role in the disease. Previous studies have reported increased MMP activity in dolichoectasia and its role in neurodegenerative and vascular processes. Targeting MMPs could prevent dolichoectasia, and reduce AD pathology, which could improve cognition. In aim 1, I injected elastase into the cisterna magna of transgenic mice for Alzheimer's disease to model dolichoectasia. To understand the contribution of dolichoectasia on AD pathology, I utilized the APPNL-G-F mice with dolichoectasia in aim 2, which showed an increase in amyloid plaque deposition, matrix metalloproteinases-9 activity (MMP-9), neuronal loss, and dysfunctional autophagy. In aim 3, I observed a decline in spatial learning and executive function along with an increase in amyloid plaque deposition and matrix metalloproteinases-2 (MMP-2) and neuronal loss in AppNL-F. I then proceeded to treat the AppNL-F x MAPT mice with doxycycline and SB-3CT to inhibit matrix metalloproteinases and observed a reduction in dolichoectasia, improvement in behavior, a reduction in AD pathology, reduction in MMP-9 activity, improvement in autophagy and preservation of neuronal cells in the CA3 hippocampal region. Therefore, I was able to see that inhibiting MMPs can cause an improvement in cognitive function in Alzheimer's disease and suggest further investigation to understand its role in the pathogenesis of the disease to help develop effective therapy. In the final chapter of my thesis, I measured TSPO in ASD participants using the [18F] FEPPA radioligand to assess neuroinflammation. I observe no increase in neuroinflammation in these individuals suggesting an atypical neuroimmune state in ASD.

English

ISBN: 9798342751933Subjects--Topical Terms:

588700
Neurosciences.
Subjects--Index Terms:

Alzheimer disease

Association Between Large Vessel (Arterial) Dilatation and Pathological Markers of Vascular Dementia and Alzheimer's Disease /
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520 $a In my thesis, we look at the association between vascular dementia and Alzheimer's disease (AD) and how vascular changes can contribute to AD pathology. AD is the pathological presence of amyloid plaque and neurofibrillary tangles, while vascular dementia is a reduction in blood flowing to the brain due to vascular impairment. In the pathogenesis for AD and vascular changes, matrix metalloproteinases (MMPs) are gaining traction to have a role in the disease. Previous studies have reported increased MMP activity in dolichoectasia and its role in neurodegenerative and vascular processes. Targeting MMPs could prevent dolichoectasia, and reduce AD pathology, which could improve cognition. In aim 1, I injected elastase into the cisterna magna of transgenic mice for Alzheimer's disease to model dolichoectasia. To understand the contribution of dolichoectasia on AD pathology, I utilized the APPNL-G-F mice with dolichoectasia in aim 2, which showed an increase in amyloid plaque deposition, matrix metalloproteinases-9 activity (MMP-9), neuronal loss, and dysfunctional autophagy. In aim 3, I observed a decline in spatial learning and executive function along with an increase in amyloid plaque deposition and matrix metalloproteinases-2 (MMP-2) and neuronal loss in AppNL-F. I then proceeded to treat the AppNL-F x MAPT mice with doxycycline and SB-3CT to inhibit matrix metalloproteinases and observed a reduction in dolichoectasia, improvement in behavior, a reduction in AD pathology, reduction in MMP-9 activity, improvement in autophagy and preservation of neuronal cells in the CA3 hippocampal region. Therefore, I was able to see that inhibiting MMPs can cause an improvement in cognitive function in Alzheimer's disease and suggest further investigation to understand its role in the pathogenesis of the disease to help develop effective therapy. In the final chapter of my thesis, I measured TSPO in ASD participants using the [18F] FEPPA radioligand to assess neuroinflammation. I observe no increase in neuroinflammation in these individuals suggesting an atypical neuroimmune state in ASD.
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