高雄醫學大學圖書館 |

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

紀錄類型:	書目-語言資料,印刷品 : 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.
提要註:	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.
Contained By:	Dissertations Abstracts International86-05B.
標題:	Behavioral psychology. -
電子資源:	http://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:

523778
Behavioral psychology.
Subjects--Index Terms:

Alzheimer disease

Association Between Large Vessel (Arterial) Dilatation and Pathological Markers of Vascular Dementia and Alzheimer's Disease /
LDR:03686nam a22004573i 4500 001 391460
005 20251124054800.5
006 m o d
007 cr|nu||||||||
008 251208s2024 miu||||||m |||||||eng d
020 $a 9798342751933
035 $a (MiAaPQD)AAI31560258
035 $a AAI31560258
040 $a MiAaPQD $b eng $c MiAaPQD $e rda
100 1 $a Simpson, Dominic, $e author. $3 523971
245 1 0 $a Association Between Large Vessel (Arterial) Dilatation and Pathological Markers of Vascular Dementia and Alzheimer's Disease / $c Dominic Simpson.
264 1 $a Ann Arbor : $b ProQuest Dissertations & Theses, $c 2024
300 $a 1 electronic resource (185 pages)
336 $a text $b txt $2 rdacontent
337 $a computer $b c $2 rdamedia
338 $a online resource $b cr $2 rdacarrier
500 $a Source: Dissertations Abstracts International, Volume: 86-05, Section: B.
500 $a Advisors: Yu, Wai Haung; Liu, Fang Committee members: McPherson, Peter.
502 $b Ph.D. $c University of Toronto (Canada) $d 2024.
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.
546 $a English
590 $a School code: 0779
650 4 $a Behavioral psychology. $3 523778
650 4 $2 96060 $a Pharmacology. $3 185640
650 4 $2 96060 $a Cognitive psychology. $3 221569
650 4 $2 96060 $a Neurosciences. $3 240374
653 $a Alzheimer disease
653 $a Cognition
653 $a Doxycycline
653 $a Matrix metalloproteinases
653 $a Vascular dementia
690 $a 0317
690 $a 0633
690 $a 0419
690 $a 0384
710 2 $a University of Toronto (Canada). $b Pharmacology. $e degree granting institution. $3 523972
720 1 $a Yu, Wai Haung $e degree supervisor.
720 1 $a Liu, Fang $e degree supervisor.
773 0 $t Dissertations Abstracts International $g 86-05B.
790 $a 0779
791 $a Ph.D.
792 $a 2024
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=31560258