語系:
繁體中文
English
說明(常見問題)
登入
回首頁
切換:
標籤
|
MARC模式
|
ISBD
The Effects of Ketones on Brain Metabolism and Cognition.
紀錄類型:
書目-語言資料,手稿 : Monograph/item
正題名/作者:
The Effects of Ketones on Brain Metabolism and Cognition./
作者:
Saito, Erin Reiko.
面頁冊數:
1 online resource (178 pages)
附註:
Source: Dissertations Abstracts International, Volume: 85-05, Section: B.
Contained By:
Dissertations Abstracts International85-05B.
標題:
Neurodegeneration. -
電子資源:
click for full text (PQDT)
ISBN:
9798380710367
The Effects of Ketones on Brain Metabolism and Cognition.
Saito, Erin Reiko.
The Effects of Ketones on Brain Metabolism and Cognition.
- 1 online resource (178 pages)
Source: Dissertations Abstracts International, Volume: 85-05, Section: B.
Thesis (Ph.D.)--Brigham Young University, 2023.
Includes bibliographical references
The brain is one of the most energetically demanding organs within the human body and is cognitively susceptible to energetic deficits such that the rise in obesity, insulin resistance, and Alzheimer's disease in recent decades pose a substantial threat to cognitive longevity. The therapeutic efficacy of ketones are well-established in epilepsy and are currently being applied to other disease states. Alzheimer's disease is characterized by impairments in brain glucose uptake and metabolism in regions relevant to learning, memory, and cognition that progress with the disease. While brain glucose uptake is impaired, ketone uptake is unaltered, potentially enabling ketones to fuel the glucose-deficient brain. Using RNA-seq data acquired from multiple publicly available AD databases, we assessed glycolytic and ketolytic gene expression in post-mortem AD and cognitively normal control brains. Gene expression was normalized to brain region - parietal lobe, cerebellum, temporal cortex, frontal lobe, inferior frontal gyrus, parahippocampal gyrus, superior temporal gyrus - and cell type - neurons, astrocytes, oligodendrocytes, and microglia. We report impairments in glycolytic gene expression in regions of the brain relevant to memory and cognition in neurons and oligodendrocytes, but not ketolytic gene expression in neurons. The data are consistent with previous work and support clinical ketone intervention.The cognitive effects of ketogenic diets remain controversial, especially in healthy adults. To elucidate the effects of a ketogenic diet in healthy mice, C57BL6 mice were placed on a ketone-supplemented ketogenic diet for eight weeks. Recognition memory was assessed in a novel object recognition test and hippocampal bioenergetics were measured using highresolution respirometry, western blot, and biochemical assays. The diet significantly improved recognition memory and enhanced hippocampal mitochondrial efficiency, measured by ATP production per unit of oxygen consumed, suggesting cognitive validity of the diet in middle-age. Long-term potentiation (LTP), the activity-dependent strengthening of synapses, within the hippocampus, is one of the molecular mechanisms of learning and memory formation. LTP of hippocampal Schaffer-collaterals was quantified in young adult C57BL/6 mice with field electrophysiology following ex vivo brain slice incubation with a β-hydroxybutyrate-rich ACSF. Mice were then placed on the ketone-supplemented diet for four weeks. Behavioral spatial memory was measured in the Morris water maze and Schaffer-collateral LTP was assessed with field electrophysiology. No meaningful changes in LTP and behavioral memory were observed with ketone treatment, suggesting ketogenic interventions may be more applicable in aging and pathologies that display cognitive deficits, rather than in healthy young adults. Together, these studies support the exploration of ketogenic interventions as a potential restorative measure in Alzheimer's disease and preventative measure in aging, which may be impactful facing the rise of obesity and insulin resistance.
Electronic reproduction.
Ann Arbor, Mich. :
ProQuest,
2024
Mode of access: World Wide Web
ISBN: 9798380710367Subjects--Topical Terms:
1472995
Neurodegeneration.
Index Terms--Genre/Form:
554714
Electronic books.
The Effects of Ketones on Brain Metabolism and Cognition.
LDR
:04388ntm a22003737 4500
001
1147299
005
20240909100750.5
006
m o d
007
cr bn ---uuuuu
008
250605s2023 xx obm 000 0 eng d
020
$a
9798380710367
035
$a
(MiAaPQ)AAI30670369
035
$a
(MiAaPQ)BrighamYoung11023
035
$a
AAI30670369
040
$a
MiAaPQ
$b
eng
$c
MiAaPQ
$d
NTU
100
1
$a
Saito, Erin Reiko.
$3
1472994
245
1 4
$a
The Effects of Ketones on Brain Metabolism and Cognition.
264
0
$c
2023
300
$a
1 online resource (178 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: 85-05, Section: B.
500
$a
Advisor: Bikman, Benjamin T.
502
$a
Thesis (Ph.D.)--Brigham Young University, 2023.
504
$a
Includes bibliographical references
520
$a
The brain is one of the most energetically demanding organs within the human body and is cognitively susceptible to energetic deficits such that the rise in obesity, insulin resistance, and Alzheimer's disease in recent decades pose a substantial threat to cognitive longevity. The therapeutic efficacy of ketones are well-established in epilepsy and are currently being applied to other disease states. Alzheimer's disease is characterized by impairments in brain glucose uptake and metabolism in regions relevant to learning, memory, and cognition that progress with the disease. While brain glucose uptake is impaired, ketone uptake is unaltered, potentially enabling ketones to fuel the glucose-deficient brain. Using RNA-seq data acquired from multiple publicly available AD databases, we assessed glycolytic and ketolytic gene expression in post-mortem AD and cognitively normal control brains. Gene expression was normalized to brain region - parietal lobe, cerebellum, temporal cortex, frontal lobe, inferior frontal gyrus, parahippocampal gyrus, superior temporal gyrus - and cell type - neurons, astrocytes, oligodendrocytes, and microglia. We report impairments in glycolytic gene expression in regions of the brain relevant to memory and cognition in neurons and oligodendrocytes, but not ketolytic gene expression in neurons. The data are consistent with previous work and support clinical ketone intervention.The cognitive effects of ketogenic diets remain controversial, especially in healthy adults. To elucidate the effects of a ketogenic diet in healthy mice, C57BL6 mice were placed on a ketone-supplemented ketogenic diet for eight weeks. Recognition memory was assessed in a novel object recognition test and hippocampal bioenergetics were measured using highresolution respirometry, western blot, and biochemical assays. The diet significantly improved recognition memory and enhanced hippocampal mitochondrial efficiency, measured by ATP production per unit of oxygen consumed, suggesting cognitive validity of the diet in middle-age. Long-term potentiation (LTP), the activity-dependent strengthening of synapses, within the hippocampus, is one of the molecular mechanisms of learning and memory formation. LTP of hippocampal Schaffer-collaterals was quantified in young adult C57BL/6 mice with field electrophysiology following ex vivo brain slice incubation with a β-hydroxybutyrate-rich ACSF. Mice were then placed on the ketone-supplemented diet for four weeks. Behavioral spatial memory was measured in the Morris water maze and Schaffer-collateral LTP was assessed with field electrophysiology. No meaningful changes in LTP and behavioral memory were observed with ketone treatment, suggesting ketogenic interventions may be more applicable in aging and pathologies that display cognitive deficits, rather than in healthy young adults. Together, these studies support the exploration of ketogenic interventions as a potential restorative measure in Alzheimer's disease and preventative measure in aging, which may be impactful facing the rise of obesity and insulin resistance.
533
$a
Electronic reproduction.
$b
Ann Arbor, Mich. :
$c
ProQuest,
$d
2024
538
$a
Mode of access: World Wide Web
650
4
$a
Neurodegeneration.
$3
1472995
650
4
$a
Insulin resistance.
$3
769352
650
4
$a
Alzheimer's disease.
$3
581461
650
4
$a
Cognition & reasoning.
$3
1372461
650
4
$a
Aging.
$3
559847
650
4
$a
Cognitive psychology.
$3
556029
650
4
$a
Neurosciences.
$3
593561
650
4
$a
Pharmaceutical sciences.
$3
1180569
650
4
$a
Psychology.
$3
555998
655
7
$a
Electronic books.
$2
local
$3
554714
690
$a
0493
690
$a
0633
690
$a
0317
690
$a
0572
690
$a
0621
710
2
$a
ProQuest Information and Learning Co.
$3
1178819
710
2
$a
Brigham Young University.
$3
1187870
773
0
$t
Dissertations Abstracts International
$g
85-05B.
856
4 0
$u
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=30670369
$z
click for full text (PQDT)
筆 0 讀者評論
多媒體
評論
新增評論
分享你的心得
Export
取書館別
處理中
...
變更密碼[密碼必須為2種組合(英文和數字)及長度為10碼以上]
登入