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Artikel ; Online: Lower GLUT1 and unchanged MCT1 in Alzheimer's disease cerebrovasculature.

Leclerc, Manon / Tremblay, Cyntia / Bourassa, Philippe / Schneider, Julie A / Bennett, David A / Calon, Frédéric

Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism

2024 , Seite(n) 271678X241237484

Abstract: The brain is a highly demanding organ, utilizing mainly glucose but also ketone bodies as sources of energy. Glucose transporter-1 (GLUT1) and monocarboxylates transporter-1 (MCT1) respectively transport glucose and ketone bodies across the blood-brain ... ...

Abstract	The brain is a highly demanding organ, utilizing mainly glucose but also ketone bodies as sources of energy. Glucose transporter-1 (GLUT1) and monocarboxylates transporter-1 (MCT1) respectively transport glucose and ketone bodies across the blood-brain barrier. While reduced glucose uptake by the brain is one of the earliest signs of Alzheimer's disease (AD), no change in the uptake of ketone bodies has been evidenced yet. To probe for changes in GLUT1 and MCT1, we performed Western immunoblotting in microvessel extracts from the parietal cortex of 60 participants of the Religious Orders Study. Participants clinically diagnosed with AD had lower cerebrovascular levels of GLUT1, whereas MCT1 remained unchanged. GLUT1 reduction was associated with lower cognitive scores. No such association was found for MCT1. GLUT1 was inversely correlated with neuritic plaques and cerebrovascular β-secretase-derived fragment levels. No other significant associations were found between both transporters, markers of Aβ and tau pathologies, sex, age at death or apolipoprotein-ε4 genotype. These results suggest that, while a deficit of GLUT1 may underlie the reduced transport of glucose to the brain in AD, no such impairment occurs for MCT1. This study thus supports the exploration of ketone bodies as an alternative energy source for the aging brain.
Sprache	Englisch
Erscheinungsdatum	2024-03-05
Erscheinungsland	United States
Dokumenttyp	Journal Article
ZDB-ID	604628-9
ISSN	1559-7016 ; 0271-678X
ISSN (online)	1559-7016
ISSN	0271-678X
DOI	10.1177/0271678X241237484
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Sex-dependent alterations in the physiology of entorhinal cortex neurons in old heterozygous 3xTg-AD mice.

Arsenault, Dany / Tremblay, Cyntia / Emond, Vincent / Calon, Frédéric

Biology of sex differences

2020 Band 11, Heft 1, Seite(n) 63

Abstract: While the higher prevalence of Alzheimer's disease (AD) in women is clear, studies suggest that biological sex may also influence AD pathogenesis. However, mechanisms behind these differences are not clear. To investigate physiological differences ... ...

Abstract	While the higher prevalence of Alzheimer's disease (AD) in women is clear, studies suggest that biological sex may also influence AD pathogenesis. However, mechanisms behind these differences are not clear. To investigate physiological differences between sexes at the cellular level in the brain, we investigated the intrinsic and synaptic properties of entorhinal cortex neurons in heterozygous 3xTg-AD mice of both sexes at the age of 20 months. This brain region was selected because of its early association with AD symptoms. First, we found physiological differences between male and female non-transgenic mice, providing indirect evidence of axonal alterations in old females. Second, we observed a transgene-dependent elevation of the firing activity, post-burst afterhyperpolarization (AHP), and spontaneous excitatory postsynaptic current (EPSC) activity, without any effect of sex. Third, the passive properties and the hyperpolarization-activated current (Ih) were altered by transgene expression only in female mice, whereas the paired-pulse ratio (PPR) of evoked EPSC was changed only in males. Fourth, both sex and transgene expression were associated with changes in action potential properties. Consistent with previous work, higher levels of Aβ neuropathology were detected in 3xTg-AD females, whereas tau deposition was similar. In summary, our results support the idea that aging and AD neuropathology differentially alter the physiology of entorhinal cortex neurons in males and females.
Mesh-Begriff(e)	ATP Binding Cassette Transporter 1/metabolism ; Aging/physiology ; Alzheimer Disease/pathology ; Alzheimer Disease/physiopathology ; Animals ; Disease Models, Animal ; Entorhinal Cortex/cytology ; Entorhinal Cortex/physiopathology ; Excitatory Postsynaptic Potentials ; Female ; Male ; Mice, Transgenic ; Neurons/physiology ; Sex Characteristics ; Synapses/physiology
Chemische Substanzen	ABCA1 protein, mouse ; ATP Binding Cassette Transporter 1
Sprache	Englisch
Erscheinungsdatum	2020-11-16
Erscheinungsland	England
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2587352-0
ISSN	2042-6410 ; 2042-6410
ISSN (online)	2042-6410
ISSN	2042-6410
DOI	10.1186/s13293-020-00337-0
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel: Evidence of Filamin A loss of solubility at the prodromal stage of neuropathologically-defined Alzheimer's disease.

Aumont, Etienne / Tremblay, Cyntia / Levert, Stéphanie / Bennett, David A / Calon, Frédéric / Leclerc, Nicole

Frontiers in aging neuroscience

2022 Band 14, Seite(n) 1038343

Abstract: Introduction: Alzheimer's disease (AD) is a multifactorial disorder diagnosed through the assessment of amyloid-beta (Aβ) and tau protein depositions. Filamin A (FLNA) could be a key partner of both Aβ and tau pathological processes and may be an ... ...

Abstract	Introduction: Alzheimer's disease (AD) is a multifactorial disorder diagnosed through the assessment of amyloid-beta (Aβ) and tau protein depositions. Filamin A (FLNA) could be a key partner of both Aβ and tau pathological processes and may be an important contributor to AD progression. The main aim of this study was to describe the differences in FLNA levels across clinicopathologic groups. Methods: From parietal cortex samples of 57 individuals (19 with no cognitive impairment (NCI), 19 mild cognitively impaired (MCI) and 19 with dementia) from the Religious Orders Study (ROS), we quantified total tau, phosphorylated tau (pTau), FLNA, synaptophysin, vesicular acetylcholine transporters (VAChT) and choline acetyltransferase (ChAT) by Western blot. Aβ42 and neuritic plaques (NP) were quantified by ELISA and Bielschowsky silver impregnation, respectively. AD staging was determined using ABC method combining Thal, Braak and the CERAD staging. From this, clinicopathologic stages of AD were established by subdividing subjects with neuropathological AD between preclinical AD, prodromal AD and AD dementia (ADD). Receiver operating characteristics analyses were performed to predict AD neuropathology from FLNA quantifications. Results: Insoluble FLNA was significantly and positively correlated with Aβ42, NP, Thal stages, ABC scores and AD clinicopathologic stages ( Discussion: We observed opposite level changes between insoluble and soluble FLNA in prodromal AD. As this stage coincides with the appearance of cognitive symptoms, this may be a key event in the transition from preclinical to prodromal AD. Insoluble FLNA could be useful to identify prodromal AD among subjects with an MCI, indicating that it might be a hallmark of prodromal AD.
Sprache	Englisch
Erscheinungsdatum	2022-11-24
Erscheinungsland	Switzerland
Dokumenttyp	Journal Article
ZDB-ID	2558898-9
ISSN	1663-4365
ISSN	1663-4365
DOI	10.3389/fnagi.2022.1038343
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Direct and Indirect Effects of Filamin A on Tau Pathology in Neuronal Cells.

Levert, Stéphanie / Pilliod, Julie / Aumont, Étienne / Armanville, Sandrine / Tremblay, Cyntia / Calon, Frédéric / Leclerc, Nicole

Molecular neurobiology

2022 Band 60, Heft 2, Seite(n) 1021–1039

Abstract: In Alzheimer disease (AD), Tau, an axonal microtubule-associated protein, becomes hyperphosphorylated, detaches from microtubules, accumulates, and self-aggregates in the somatodendritic (SD) compartment. The accumulation of hyperphosphorylated and ... ...

Abstract	In Alzheimer disease (AD), Tau, an axonal microtubule-associated protein, becomes hyperphosphorylated, detaches from microtubules, accumulates, and self-aggregates in the somatodendritic (SD) compartment. The accumulation of hyperphosphorylated and aggregated Tau is also seen in other neurodegenerative diseases such as frontotemporal lobar degeneration (FTLD-Tau). Previous studies reported a link between filamin A (FLNA), an actin-binding protein found in the SD compartment, and Tau pathology. In the present study, we further explored this link. We confirmed the interaction of Tau with FLNA in neuroblastoma 2a (N2a) cells. This interaction was mediated by a domain located between the 157 and 383 amino acids (a.a.) of Tau. Our results also revealed that the overexpression of FLNA resulted in an intracellular accumulation of wild-type Tau and Tau mutants (P301L, V337M, and R406W) in N2a cells. Tau phosphorylation and cleavage by caspase-3 but not its aggregation were increased upon FLNA overexpression in N2a cells. In the parietal cortex of AD brain, insoluble FLNA was increased compared to control brain, but it did not correlate with Tau pathology. Interestingly, Tau binding to microtubules and F-actin was preserved upon FLNA overexpression in N2a cells. Lastly, our results revealed that FLNA also induced the accumulation of annexin A2, a Tau interacting partner involved in its axonal localization. Collectively, our data indicated that in Tauopathies, FLNA could contribute to Tau pathology by acting on Tau and annexin A2.
Mesh-Begriff(e)	Alzheimer Disease/pathology ; Annexin A2/metabolism ; Filamins/metabolism ; Frontotemporal Lobar Degeneration/pathology ; Neurons/metabolism ; Phosphorylation ; tau Proteins/metabolism ; Tauopathies/metabolism ; Animals ; Mice
Chemische Substanzen	Annexin A2 ; Filamins ; tau Proteins ; FlnA protein, mouse
Sprache	Englisch
Erscheinungsdatum	2022-11-18
Erscheinungsland	United States
Dokumenttyp	Journal Article
ZDB-ID	645020-9
ISSN	1559-1182 ; 0893-7648
ISSN (online)	1559-1182
ISSN	0893-7648
DOI	10.1007/s12035-022-03121-w
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Higher angiotensin-converting enzyme 2 (ACE2) levels in the brain of individuals with Alzheimer's disease.

Reveret, Louise / Leclerc, Manon / Emond, Vincent / Tremblay, Cyntia / Loiselle, Andréanne / Bourassa, Philippe / Bennett, David A / Hébert, Sébastien S / Calon, Frédéric

Acta neuropathologica communications

2023 Band 11, Heft 1, Seite(n) 159

Abstract: Cognitive decline due to Alzheimer's disease (AD) is frequent in the geriatric population, which has been disproportionately affected by the COVID-19 pandemic. In this study, we investigated the levels of angiotensin-converting enzyme 2 (ACE2), a ... ...

Abstract	Cognitive decline due to Alzheimer's disease (AD) is frequent in the geriatric population, which has been disproportionately affected by the COVID-19 pandemic. In this study, we investigated the levels of angiotensin-converting enzyme 2 (ACE2), a regulator of the renin-angiotensin system and the main entry receptor of SARS-CoV-2 in host cells, in postmortem parietal cortex samples from two independent AD cohorts, totalling 142 persons. Higher concentrations of ACE2 protein (p < 0.01) and mRNA (p < 0.01) were found in individuals with a neuropathological diagnosis of AD compared to age-matched healthy control subjects. Brain levels of soluble ACE2 were inversely associated with cognitive scores (p = 0.02) and markers of pericytes (PDGFRβ, p = 0.02 and ANPEP, p = 0.007), but positively correlated with concentrations of soluble amyloid-β peptides (Aβ) (p = 0.01) and insoluble phospho-tau (S396/404, p = 0.002). However, no significant differences in ACE2 were observed in the 3xTg-AD mouse model of tau and Aβ neuropathology. Results from immunofluorescence and Western blots showed that ACE2 protein is predominantly localized in microvessels in the mouse brain whereas it is more frequently found in neurons in the human brain. The present data suggest that higher levels of soluble ACE2 in the human brain may contribute to AD, but their role in CNS infection by SARS-CoV-2 remains unclear.
Mesh-Begriff(e)	Aged ; Mice ; Animals ; Humans ; Alzheimer Disease/pathology ; Angiotensin-Converting Enzyme 2 ; Pandemics ; COVID-19 ; SARS-CoV-2/metabolism ; Brain/pathology
Chemische Substanzen	Angiotensin-Converting Enzyme 2 (EC 3.4.17.23)
Sprache	Englisch
Erscheinungsdatum	2023-10-02
Erscheinungsland	England
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2715589-4
ISSN	2051-5960 ; 2051-5960
ISSN (online)	2051-5960
ISSN	2051-5960
DOI	10.1186/s40478-023-01647-1
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Correction to: Higher angiotensin‑converting enzyme 2 (ACE2) levels in the brain of individuals with Alzheimer's disease.

Reveret, Louise / Leclerc, Manon / Emond, Vincent / Tremblay, Cyntia / Loiselle, Andréanne / Bourassa, Philippe / Bennett, David A / Hébert, Sébastien S / Calon, Frédéric

Acta neuropathologica communications

2023 Band 11, Heft 1, Seite(n) 173

Sprache	Englisch
Erscheinungsdatum	2023-11-01
Erscheinungsland	England
Dokumenttyp	Published Erratum
ZDB-ID	2715589-4
ISSN	2051-5960 ; 2051-5960
ISSN (online)	2051-5960
ISSN	2051-5960
DOI	10.1186/s40478-023-01678-8
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Age-dependent impact of streptozotocin on metabolic endpoints and Alzheimer's disease pathologies in 3xTg-AD mice.

Canet, Geoffrey / Gratuze, Maud / Zussy, Charleine / Bouali, Mohamed Lala / Diaz, Sofia Diego / Rocaboy, Emma / Laliberté, Francis / El Khoury, Noura B / Tremblay, Cyntia / Morin, Françoise / Calon, Frédéric / Hébert, Sébastien S / Julien, Carl / Planel, Emmanuel

Neurobiology of disease

2024 , Seite(n) 106526

Abstract: Alzheimer's disease (AD) is a multifactorial neurodegenerative disease with a complex origin, thought to involve a combination of genetic, biological and environmental factors. Insulin dysfunction has emerged as a potential factor contributing to AD ... ...

Abstract	Alzheimer's disease (AD) is a multifactorial neurodegenerative disease with a complex origin, thought to involve a combination of genetic, biological and environmental factors. Insulin dysfunction has emerged as a potential factor contributing to AD pathogenesis, particularly in individuals with diabetes, and among those with insulin deficiency or undergoing insulin therapy. The intraperitoneal administration of streptozotocin (STZ) is a widely used rodent model to explore the impact of insulin deficiency on AD pathology, although prior research predominantly focused on young animals, with no comparative analysis across different age groups. Our study aimed to fill this gap by analyzing the impact of insulin dysfunction in 7 and 23 months 3xTg-AD mice, that exhibit both amyloid and tau pathologies. Our objective was to elucidate the age-specific consequences of insulin deficiency on AD pathology. STZ administration led to insulin deficiency in the younger mice, resulting in an increase in cortical amyloid-β (Aβ) and tau aggregation, while tau phosphorylation was not significantly affected. Conversely, older mice displayed an unexpected resilience to the peripheral metabolic impact of STZ, while exhibiting an increase in both tau phosphorylation and aggregation without significantly affecting amyloid pathology. These changes were paralleled with alterations in signaling pathways involving tau kinases and phosphatases. Several markers of blood-brain barrier (BBB) integrity declined with age in 3xTg-AD mice, which might facilitate a direct neurotoxic effect of STZ in older mice. Overall, our research confirms the influence of insulin signaling dysfunction on AD pathology, but also advises careful interpretation of data related to STZ-induced effects in older animals.
Sprache	Englisch
Erscheinungsdatum	2024-05-09
Erscheinungsland	United States
Dokumenttyp	Journal Article
ZDB-ID	1211786-9
ISSN	1095-953X ; 0969-9961
ISSN (online)	1095-953X
ISSN	0969-9961
DOI	10.1016/j.nbd.2024.106526
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Cerebrovascular insulin receptors are defective in Alzheimer's disease.

Leclerc, Manon / Bourassa, Philippe / Tremblay, Cyntia / Caron, Vicky / Sugère, Camille / Emond, Vincent / Bennett, David A / Calon, Frédéric

Brain : a journal of neurology

2022 Band 146, Heft 1, Seite(n) 75–90

Abstract: Central response to insulin is suspected to be defective in Alzheimer's disease. As most insulin is secreted in the bloodstream by the pancreas, its capacity to regulate brain functions must, at least partly, be mediated through the cerebral vasculature. ...

Abstract	Central response to insulin is suspected to be defective in Alzheimer's disease. As most insulin is secreted in the bloodstream by the pancreas, its capacity to regulate brain functions must, at least partly, be mediated through the cerebral vasculature. However, how insulin interacts with the blood-brain barrier and whether alterations of this interaction could contribute to Alzheimer's disease pathophysiology both remain poorly defined. Here, we show that human and murine cerebral insulin receptors (INSRs), particularly the long isoform INSRα-B, are concentrated in microvessels rather than in the parenchyma. Vascular concentrations of INSRα-B were lower in the parietal cortex of subjects diagnosed with Alzheimer's disease, positively correlating with cognitive scores, leading to a shift towards a higher INSRα-A/B ratio, consistent with cerebrovascular insulin resistance in the Alzheimer's disease brain. Vascular INSRα was inversely correlated with amyloid-β plaques and β-site APP cleaving enzyme 1, but positively correlated with insulin-degrading enzyme, neprilysin and P-glycoprotein. Using brain cerebral intracarotid perfusion, we found that the transport rate of insulin across the blood-brain barrier remained very low (<0.03 µl/g·s) and was not inhibited by an insulin receptor antagonist. However, intracarotid perfusion of insulin induced the phosphorylation of INSRβ that was restricted to microvessels. Such an activation of vascular insulin receptor was blunted in 3xTg-AD mice, suggesting that Alzheimer's disease neuropathology induces insulin resistance at the level of the blood-brain barrier. Overall, the present data in post-mortem Alzheimer's disease brains and an animal model of Alzheimer's disease indicate that defects in the insulin receptor localized at the blood-brain barrier strongly contribute to brain insulin resistance in Alzheimer's disease, in association with β-amyloid pathology.
Mesh-Begriff(e)	Humans ; Mice ; Animals ; Alzheimer Disease/pathology ; Receptor, Insulin ; Insulin Resistance ; Amyloid beta-Peptides/metabolism ; Brain/pathology ; Insulin/pharmacology ; Disease Models, Animal
Chemische Substanzen	Receptor, Insulin (EC 2.7.10.1) ; Amyloid beta-Peptides ; Insulin
Sprache	Englisch
Erscheinungsdatum	2022-10-15
Erscheinungsland	England
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80072-7
ISSN	1460-2156 ; 0006-8950
ISSN (online)	1460-2156
ISSN	0006-8950
DOI	10.1093/brain/awac309
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Inhibition of PLK2 activity affects APP and tau pathology and improves synaptic content in a sex-dependent manner in a 3xTg mouse model of Alzheimer's disease.

Martínez-Drudis, Laura / Sheta, Razan / Pellegrinato, Rémi / Loukili, Salma / Tremblay, Cyntia / Calon, Frédéric / Rivest, Serge / Oueslati, Abid

Neurobiology of disease

2022 Band 172, Seite(n) 105833

Abstract: Converging lines of evidence suggest that abnormal accumulation of the kinase Polo-like kinase 2 (PLK2) might play a role in the pathogenesis of Alzheimer's disease (AD), possibly through its role in regulating the amyloid β (Aβ) cascade. In the present ... ...

Abstract	Converging lines of evidence suggest that abnormal accumulation of the kinase Polo-like kinase 2 (PLK2) might play a role in the pathogenesis of Alzheimer's disease (AD), possibly through its role in regulating the amyloid β (Aβ) cascade. In the present study, we investigated the effect of inhibiting PLK2 kinase activity in in vitro and in vivo models of AD neuropathology. First, we confirmed that PLK2 overexpression modulated APP and Tau protein levels and phosphorylation in cell culture, in a kinase activity dependent manner. Furthermore, a transient treatment of triple transgenic mouse model of AD (3xTg-AD) with a potent and specific PLK2 pharmacological inhibitor (PLK2i #37) reduced some neuropathological aspects in a sex-dependent manner. In 3xTg-AD males, treatment with PLK2i #37 led to lower Tau burden, higher synaptic protein content, and prevented learning and memory deficits. In contrast, treated females showed an exacerbation of Tau pathology, associated with a reduction in amyloid plaque accumulation. Overall, our findings suggest that PLK2 inhibition alters key components of AD neuropathology in a sex-dependent manner and might display a therapeutic potential for the treatment for AD and related dementia.
Mesh-Begriff(e)	Alzheimer Disease/metabolism ; Amyloid beta-Peptides/metabolism ; Amyloid beta-Protein Precursor/genetics ; Amyloid beta-Protein Precursor/metabolism ; Animals ; Disease Models, Animal ; Female ; Male ; Mice ; Mice, Transgenic ; Plaque, Amyloid/pathology ; tau Proteins/metabolism
Chemische Substanzen	Amyloid beta-Peptides ; Amyloid beta-Protein Precursor ; tau Proteins
Sprache	Englisch
Erscheinungsdatum	2022-07-26
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1211786-9
ISSN	1095-953X ; 0969-9961
ISSN (online)	1095-953X
ISSN	0969-9961
DOI	10.1016/j.nbd.2022.105833
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Higher Angiotensin I Converting Enzyme 2 (ACE2) levels in the brain of individuals with Alzheimer's disease.

Reveret, Louise / Leclerc, Manon / Emond, vincent / Loiselle, Andreanne / Philippe, Bourassa / Tremblay, Cyntia / Bennett, David A / Hebert, Sebastien S. / Calon, Frederic S.

bioRxiv

Abstract: The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a major cause of death in the elderly. Cognitive decline due to Alzheimer9s disease (AD) is frequent in the geriatric population disproportionately affected by the COVID-19 pandemic. ... ...

Abstract	The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a major cause of death in the elderly. Cognitive decline due to Alzheimer9s disease (AD) is frequent in the geriatric population disproportionately affected by the COVID-19 pandemic. Interestingly, central nervous system (CNS) manifestations have been reported in SARS-CoV-2-infected patients. In this study, we investigated the levels of Angiotensin I Converting Enzyme 2 (ACE2), the main entry receptor of SARS-COV-2 in cells, in postmortem parietal cortex samples from two independent AD cohorts, totalling 142 persons. Higher concentrations of ACE2 protein and mRNA were found in individuals with a neuropathological diagnosis of AD compared to age-matched healthy control subjects. Brain levels of soluble ACE2 were inversely associated with cognitive scores (p = 0.02), markers of pericytes (PDGFRβ, p=0.02 and ANPEP, p = 0.007) and caveolin1 (p = 0.03), but positively correlated with soluble amyloid-β peptides (Aβ) concentrations (p = 0.01) and insoluble phospho-tau (S396/404, p = 0.002). No significant differences in ACE2 were observed in the 3xTgAD mouse model of tau and Aβ neuropathology. Results from immunofluorescence and Western blots showed that ACE2 protein is mainly localized in neurons in the human brain but predominantly in microvessels in the mouse brain. The present data show that an AD diagnosis is associated with higher levels of soluble ACE2 in the human brain, which might contribute to a higher risk of CNS SARS-CoV-2 infection.
Schlagwörter	covid19
Sprache	Englisch
Erscheinungsdatum	2023-01-18
Verlag	Cold Spring Harbor Laboratory
Dokumenttyp	Artikel ; Online
DOI	10.1101/2023.01.17.524254
Datenquelle	COVID19

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