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Book: The handbook of Alzheimer's disease and other dementias

Budson, Andrew E. / Kowall, Neil W.

(Wiley-Blackwell handbooks of behavioral neuroscience)

2011

Author's details	ed. by Andrew E. Budson and Neil W. Kowall
Series title	Wiley-Blackwell handbooks of behavioral neuroscience
Keywords	Dementia
Language	English
Size	XIV, 629 S., [8] Bl. : Ill., graph. Darst.
Publisher	Wiley-Blackwell
Publishing place	Malden, Mass
Publishing country	United States
Document type	Book
HBZ-ID	HT017009587
ISBN	978-1-4051-6828-1 ; 1-4051-6828-5
Database	Catalogue ZB MED Medicine, Health

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Article ; Online: Near-Infrared Optical Spectroscopy In Vivo Distinguishes Subjects with Alzheimer's Disease from Age-Matched Controls.

Greco, Frank A / McKee, Ann C / Kowall, Neil W / Hanlon, Eugene B

Journal of Alzheimer's disease : JAD

2021 Volume 82, Issue 2, Page(s) 791–802

Abstract: Background: Medical imaging methods such as PET and MRI aid clinical assessment of Alzheimer's disease (AD). Less expensive, less technically demanding, and more widely deployable technologies are needed to expand objective screening for diagnosis, ... ...

Abstract	Background: Medical imaging methods such as PET and MRI aid clinical assessment of Alzheimer's disease (AD). Less expensive, less technically demanding, and more widely deployable technologies are needed to expand objective screening for diagnosis, treatment, and research. We previously reported brain tissue near-infrared optical spectroscopy (NIR) in vitro indicating the potential to meet this need. Objective: To determine whether completely non-invasive, clinical, NIR in vivo can distinguish AD patients from age-matched controls and to show the potential of NIR as a clinical screen and monitor of therapeutic efficacy. Methods: NIR spectra were acquired in vivo. Three groups were studied: autopsy-confirmed AD, control and mild cognitive impairment (MCI). A feature selection approach using the first derivative of the intensity normalized spectra was used to discover spectral regions that best distinguished "AD-alone" (i.e., without other significant neuropathology) from controls. The approach was then applied to other autopsy-confirmed AD cases and to clinically diagnosed MCI cases. Results: Two regions about 860 and 895 nm completely separate AD patients from controls and differentiate MCI subjects according to the degree of impairment. The 895 nm feature is more important in separating MCI subjects from controls (ratio-of-weights: 1.3); the 860 nm feature is more important for distinguishing MCI from AD (ratio-of-weights: 8.2). Conclusion: These results form a proof of the concept that near-infrared spectroscopy can detect and classify diseased and normal human brain in vivo. A clinical trial is needed to determine whether the two features can track disease progression and monitor potential therapeutic interventions.
Language	English
Publishing date	2021-06-06
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1440127-7
ISSN	1875-8908 ; 1387-2877
ISSN (online)	1875-8908
ISSN	1387-2877
DOI	10.3233/JAD-201021
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Article ; Online: Annualized changes in rate of amyloid deposition and neurodegeneration are greater in participants who become amyloid positive than those who remain amyloid negative.

Groechel, Renée C / Tripodis, Yorghos / Alosco, Michael L / Mez, Jesse / Qiu, Wei Qiao / Mercier, Gustavo / Goldstein, Lee / Budson, Andrew E / Kowall, Neil W / Killiany, Ronald J

Neurobiology of aging

2023 Volume 127, Page(s) 33–42

Abstract: This study longitudinally examined participants in the Alzheimer's Disease Neuroimaging Initiative (ADNI) who underwent a conversion in amyloid-beta (Aβ) status in comparison to a group of ADNI participants who did not show a change in amyloid status ... ...

Abstract	This study longitudinally examined participants in the Alzheimer's Disease Neuroimaging Initiative (ADNI) who underwent a conversion in amyloid-beta (Aβ) status in comparison to a group of ADNI participants who did not show a change in amyloid status over the same follow-up period. Participants included 136 ADNI dementia-free participants with 2 florbetapir positron emission tomography (PET) scans. Of these participants, 68 showed amyloid conversion as measured on florbetapir PET, and the other 68 did not. Amyloid converters and non-converters were chosen to have representative demographic data (age, education, sex, diagnostic status, and race). The amyloid converter group showed increased prevalence of APOE ε4 (p < 0.001), greater annualized percent volume loss in selected magnetic resonance imaging (MRI) regions (p < 0.05), lower cerebrospinal fluid Aβ
MeSH term(s)	Humans ; Alzheimer Disease/pathology ; Aniline Compounds ; Ethylene Glycols ; Amyloid beta-Peptides/metabolism ; Positron-Emission Tomography/methods ; Cognitive Dysfunction/pathology ; Amyloid ; Brain/metabolism
Chemical Substances	florbetapir (6867Q6IKOD) ; Aniline Compounds ; Ethylene Glycols ; Amyloid beta-Peptides ; Amyloid
Language	English
Publishing date	2023-03-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	604505-4
ISSN	1558-1497 ; 0197-4580
ISSN (online)	1558-1497
ISSN	0197-4580
DOI	10.1016/j.neurobiolaging.2023.03.005
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Zs.A 1685: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Biomarkers of Alzheimer's disease in Black and/or African American Alzheimer's Disease Neuroimaging Initiative (ADNI) participants.

Groechel, Renée C / Tripodis, Yorghos / Alosco, Michael L / Mez, Jesse / Qiao Qiu, Wei / Goldstein, Lee / Budson, Andrew E / Kowall, Neil W / Shaw, Leslie M / Weiner, Michael / Jack, Clifford R / Killiany, Ronald J

Neurobiology of aging

2023 Volume 131, Page(s) 144–152

Abstract: Majority of dementia research is conducted in non-Hispanic White participants despite a greater prevalence of dementia in other racial groups. To obtain a better understanding of biomarker presentation of Alzheimer's disease (AD) in the non-Hispanic ... ...

Abstract	Majority of dementia research is conducted in non-Hispanic White participants despite a greater prevalence of dementia in other racial groups. To obtain a better understanding of biomarker presentation of Alzheimer's disease (AD) in the non-Hispanic White population, this study exclusively examined AD biomarker abnormalities in 85 Black and/or African American participants within the Alzheimer's Disease Neuroimaging Initiative (ADNI). Participants were classified by the ADNI into 3 clinical groups: cognitively normal, mild cognitive impairment, or dementia. Data examined included demographics, apolipoprotein E (APOE) ε4, cerebrospinal fluid (CSF) Aβ
MeSH term(s)	Humans ; Black or African American ; Alzheimer Disease/diagnostic imaging ; Black People ; Neuroimaging ; Apolipoprotein E4 ; Biomarkers
Chemical Substances	Apolipoprotein E4 ; Biomarkers
Language	English
Publishing date	2023-07-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	604505-4
ISSN	1558-1497 ; 0197-4580
ISSN (online)	1558-1497
ISSN	0197-4580
DOI	10.1016/j.neurobiolaging.2023.07.021
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Zs.A 1685: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Cortical-sparing chronic traumatic encephalopathy (CSCTE): a distinct subtype of CTE.

Acta neuropathologica

2024 Volume 147, Issue 1, Page(s) 45

Abstract: Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease caused by repetitive head impacts (RHI) and pathologically defined as neuronal phosphorylated tau aggregates around small blood vessels and concentrated at sulcal depths. Cross- ... ...

Abstract	Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease caused by repetitive head impacts (RHI) and pathologically defined as neuronal phosphorylated tau aggregates around small blood vessels and concentrated at sulcal depths. Cross-sectional studies suggest that tau inclusions follow a stereotyped pattern that begins in the neocortex in low stage disease, followed by involvement of the medial temporal lobe and subcortical regions with significant neocortical burden in high stage CTE. Here, we define a subset of brain donors with high stage CTE and with a low overall cortical burden of tau inclusions (mean semiquantitative value ≤1) and classify them as cortical-sparing CTE (CSCTE). Of 620 brain donors with pathologically diagnosed CTE, 66 (11%) met criteria for CSCTE. Compared to typical high stage CTE, those with CSCTE had a similar age at death and years of contact sports participation and were less likely to carry apolipoprotein ε4 (p < 0.05). CSCTE had less overall tau pathology severity, but a proportional increase of disease burden in medial temporal lobe and brainstem regions compared to the neocortex (p's < 0.001). CSCTE also had lower prevalence of comorbid neurodegenerative disease. Clinically, CSCTE participants were less likely to have dementia (p = 0.023) and had less severe cognitive difficulties (as reported by informants using the Functional Activities Questionnaire (FAQ); p < 0.001, meta-cognitional index T score; p = 0.002 and Cognitive Difficulties Scale (CDS); p < 0.001,) but had an earlier onset age of behavioral (p = 0.006) and Parkinsonian motor (p = 0.013) symptoms when compared to typical high stage CTE. Other comorbid tauopathies likely contributed in part to these differences: when cases with concurrent Alzheimer dementia or frontal temporal lobar degeneration with tau pathology were excluded, differences were largely retained, but only remained significant for FAQ (p = 0.042), meta-cognition index T score (p = 0.014) and age of Parkinsonian motor symptom onset (p = 0.046). Overall, CSCTE appears to be a distinct subtype of high stage CTE with relatively greater involvement of subcortical and brainstem regions and less severe cognitive symptoms.
MeSH term(s)	Humans ; Chronic Traumatic Encephalopathy ; Neurodegenerative Diseases ; Cross-Sectional Studies ; Brain ; Alzheimer Disease
Language	English
Publishing date	2024-02-26
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1079-0
ISSN	1432-0533 ; 0001-6322
ISSN (online)	1432-0533
ISSN	0001-6322
DOI	10.1007/s00401-024-02690-5
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Article ; Online: Modulation of histone H3K4 dimethylation by spermidine ameliorates motor neuron survival and neuropathology in a mouse model of ALS.

Choi, Seung-Hye / Yousefian-Jazi, Ali / Hyeon, Seung Jae / Nguyen, Phuong Thi Thanh / Chu, Jiyeon / Kim, Sojung / Kim, Suhyun / Ryu, Hannah L / Kowall, Neil W / Ryu, Hoon / Lee, Junghee

Journal of biomedical science

2022 Volume 29, Issue 1, Page(s) 106

Abstract: Background: Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder characterized by progressive paralysis due to motor neuron degeneration. It has been proposed that epigenetic modification and transcriptional dysregulation may ... ...

Abstract	Background: Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder characterized by progressive paralysis due to motor neuron degeneration. It has been proposed that epigenetic modification and transcriptional dysregulation may contribute to motor neuron death. In this study, we investigate the basis for therapeutic approaches to target lysine-specific histone demethylase 1 (LSD1) and elucidate the mechanistic role of LSD1-histone H3K4 signaling pathway in ALS pathogenesis. Methods: In order to examine the role of spermidine (SD), we administered SD to an animal model of ALS (G93A) and performed neuropathological analysis, body weight, and survival evaluation. Results: Herein, we found that LSD1 activity is increased while levels of H3K4me2, a substrate of LSD1, is decreased in cellular and animal models of ALS. SD administration modulated the LSD1 activity and restored H3K4me2 levels in ChAT-positive motor neurons in the lumbar spinal cord of ALS mice. SD prevented cellular damage by improving the number and size of motor neurons in ALS mice. SD administration also reduced GFAP-positive astrogliogenesis in the white and gray matter of the lumbar spinal cord, improving the neuropathology of ALS mice. Moreover, SD administration improved the rotarod performance and gait analysis of ALS mice. Finally, SD administration delayed disease onset and prolonged the lifespan of ALS (G93A) transgenic mice. Conclusion: Together, modulating epigenetic targets such as LSD1 by small compounds may be a useful therapeutic strategy for treating ALS.
MeSH term(s)	Mice ; Animals ; Amyotrophic Lateral Sclerosis/metabolism ; Spermidine/metabolism ; Spermidine/therapeutic use ; Histones/metabolism ; Superoxide Dismutase ; Motor Neurons ; Spinal Cord/metabolism ; Spinal Cord/pathology ; Mice, Transgenic ; Disease Models, Animal
Chemical Substances	Spermidine (U87FK77H25) ; Histones ; Superoxide Dismutase (EC 1.15.1.1)
Language	English
Publishing date	2022-12-20
Publishing country	England
Document type	Journal Article
ZDB-ID	1193378-1
ISSN	1423-0127 ; 1021-7770
ISSN (online)	1423-0127
ISSN	1021-7770
DOI	10.1186/s12929-022-00890-3
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Book: The handbook of Alzheimer's disease and other dementias

Budson, Andrew E / Kowall, Neil W

(Wiley-Blackwell handbooks of behavioral neuroscience)

2011

Author's details	edited by Andrew E. Budson and Neil W. Kowall
Series title	Wiley-Blackwell handbooks of behavioral neuroscience
MeSH term(s)	Dementia
Language	English
Size	xiv, 629 p. :, ill.
Publisher	Wiley-Blackwell
Publishing place	Chichester, West Sussex, UK
Document type	Book
ISBN	9781405168281 ; 9781444344080 ; 9781444344103 ; 9781444344097 ; 1405168285 ; 1444344080 ; 1444344102 ; 1444344099
Database	Catalogue of the US National Library of Medicine (NLM)

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Article ; Online: Dual dose-dependent effects of fingolimod in a mouse model of Alzheimer's disease.

Carreras, Isabel / Aytan, Nurgul / Choi, Ji-Kyung / Tognoni, Christina M / Kowall, Neil W / Jenkins, Bruce G / Dedeoglu, Alpaslan

Scientific reports

2019 Volume 9, Issue 1, Page(s) 10972

Abstract: Lipid metabolism is abnormal in Alzheimer's disease (AD) brain leading to ceramide and sphingosine accumulation and reduced levels of brain sphingosine-1-phosphate (S1P). We hypothesize that changes in S1P signaling are central to the inflammatory and ... ...

Abstract	Lipid metabolism is abnormal in Alzheimer's disease (AD) brain leading to ceramide and sphingosine accumulation and reduced levels of brain sphingosine-1-phosphate (S1P). We hypothesize that changes in S1P signaling are central to the inflammatory and immune-pathogenesis of AD and the therapeutic benefits of fingolimod, a structural analog of sphingosine that is FDA approved for the treatment of multiple sclerosis. We recently reported that the neuroprotective effects of fingolimod in 5xFAD transgenic AD mice treated from 1-3 months of age were greater at 1 mg/kg/day than at 5 mg/kg/day. Here we performed a dose-response study using fingolimod from 0.03 to 1 mg/kg/day in 5xFAD mice treated from 1-8 months of age. At 1 mg/kg/day, fingolimod decreased both peripheral blood lymphocyte counts and brain Aβ levels, but at the lowest dose tested (0.03 mg/kg/day), we detected improved memory, decreased activation of brain microglia and astrocytes, and restored hippocampal levels of GABA and glycerophosphocholine with no effect on circulating lymphocyte counts. These findings suggests that, unlike the case in multiple sclerosis, fingolimod may potentially have therapeutic benefits in AD at low doses that do not affect peripheral lymphocyte function.
MeSH term(s)	Alzheimer Disease/drug therapy ; Amyloid beta-Peptides/metabolism ; Animals ; Astrocytes/drug effects ; Astrocytes/pathology ; Brain/drug effects ; Brain/pathology ; Disease Models, Animal ; Drug Repositioning ; Female ; Fingolimod Hydrochloride/administration & dosage ; Fingolimod Hydrochloride/therapeutic use ; Mice ; Mice, Transgenic ; Microglia/drug effects ; Microglia/pathology ; Neuroprotective Agents/administration & dosage ; gamma-Aminobutyric Acid/metabolism
Chemical Substances	Amyloid beta-Peptides ; Neuroprotective Agents ; gamma-Aminobutyric Acid (56-12-2) ; Fingolimod Hydrochloride (G926EC510T)
Language	English
Publishing date	2019-07-29
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-019-47287-1
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Metabolomic Analysis Identifies Alterations of Amino Acid Metabolome Signatures in the Postmortem Brain of Alzheimer's Disease.

Kim, Yoon Hwan / Shim, Hyun Soo / Kim, Kyoung Heon / Lee, Junghee / Chung, Bong Chul / Kowall, Neil W / Ryu, Hoon / Lee, Jeongae

Experimental neurobiology

2019 Volume 28, Issue 3, Page(s) 376–389

Abstract: Despite significant advances in neuroscience research over the past several decades, the exact cause of AD has not yet fully understood. The metabolic hypothesis as well as the amyloid and tau hypotheses have been proposed to be associated with AD ... ...

Abstract	Despite significant advances in neuroscience research over the past several decades, the exact cause of AD has not yet fully understood. The metabolic hypothesis as well as the amyloid and tau hypotheses have been proposed to be associated with AD pathogenesis. In order to identify metabolome signatures from the postmortem brains of sporadic AD patients and control subjects, we performed ultra performance liquid chromatography coupled with linear ion trap-Orbitrap mass spectrometer (UPLC-LTQ-Orbitrap-MS). Not only our study identified new metabolome signatures but also verified previously known metabolome profiles in the brain. Statistical modeling of the analytical data and validation of the structural assignments discovered metabolic biomarkers associated with the AD pathogenesis. Interestingly, hypotaurin, myo-inositol and oxo-proline levels were markedly elevated in AD while lutamate and N-acetyl-aspartate were decreased in the postmortem brain tissue of AD patients. In addition, neurosteroid level such as cortisol was significantly increased in AD. Together, our data indicate that impaired amino acid metabolism is associated with AD pathogenesis and the altered amino acid signatures can be useful diagnostic biomarkers of AD. Thus, modulation of amino acid metabolism may be a possible therapeutic approach to treat AD.
Language	English
Publishing date	2019-06-26
Publishing country	Korea (South)
Document type	Journal Article
ZDB-ID	2639017-6
ISSN	2093-8144 ; 1226-2560
ISSN (online)	2093-8144
ISSN	1226-2560
DOI	10.5607/en.2019.28.3.376
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Article ; Online: Lack of Association of Informant-Reported Traumatic Brain Injury and Chronic Traumatic Encephalopathy.

Culhane, Julia E / Jackson, Colleen E / Tripodis, Yorghos / Nowinski, Christopher J / Dams-O'Connor, Kristen / Pettway, Erika / Uretsky, Madeline / Abdolmohammadi, Bobak / Nair, Evan / Martin, Brett / Palmisano, Joseph / Katz, Douglas I / Dwyer, Brigid / Daneshvar, Daniel H / Goldstein, Lee E / Kowall, Neil W / Cantu, Robert C / Stern, Robert A / Huber, Bertrand Russell /

Crary, John F / Mez, Jesse / Stein, Thor D / McKee, Ann C / Alosco, Michael L

Journal of neurotrauma

2024

Abstract: Repetitive head impacts (RHIs) from football are associated with the neurodegenerative tauopathy chronic traumatic encephalopathy (CTE). It is unclear whether a history of traumatic brain injury (TBI) is sufficient to precipitate CTE neuropathology. We ... ...

Abstract	Repetitive head impacts (RHIs) from football are associated with the neurodegenerative tauopathy chronic traumatic encephalopathy (CTE). It is unclear whether a history of traumatic brain injury (TBI) is sufficient to precipitate CTE neuropathology. We examined the association between TBI and CTE neuropathology in 580 deceased individuals exposed to RHIs from football. TBI history was assessed using a modified version of the Ohio State University TBI Identification Method Short Form administered to informants. There were 22 donors who had no TBI, 213 who had at least one TBI without loss of consciousness (LOC), 345 who had TBI with LOC, and, of those with a history of TBI with LOC, 36 who had at least one moderate-to-severe TBI (msTBI, LOC >30 min). CTE neuropathology was diagnosed in 405. There was no association between CTE neuropathology status or severity and TBI with LOC (odds ratio [OR] = 0.95, 95% confidence interval [CI] = 0.64-1.41; OR = 1.22, 95% CI = 0.71-2.09) or msTBI (OR = 0.70, 95% CI = 0.33-1.50; OR = 1.01, 95% CI = 0.30-3.41). There were no associations with other neurodegenerative or cerebrovascular pathologies examined. TBI with LOC and msTBI were not associated with CTE neuropathology in this sample of brain donors exposed to RHIs from American football.
Language	English
Publishing date	2024-04-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	645092-1
ISSN	1557-9042 ; 0897-7151
ISSN (online)	1557-9042
ISSN	0897-7151
DOI	10.1089/neu.2023.0391
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