scholarly journals Differential Effects of ApoE Isoforms on Dendritic Spines In Vivo: Linking an Alzheimer's Disease Risk Factor with Synaptic Alterations

2010 ◽  
Vol 30 (13) ◽  
pp. 4526-4527 ◽  
Author(s):  
J. M. Basak ◽  
J. Kim
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Factor ◽  
Dendritic Spines ◽  
Disease Risk ◽  
Disease Risk Factor ◽  
Differential Effects ◽  
Apoe Isoforms

scholarly journals Alzheimer's Disease Risk Factor Pyk2 Mediates Amyloid-β-Induced Synaptic Dysfunction and Loss

2018 ◽  
Vol 39 (4) ◽  
pp. 758-772 ◽  
Author(s):  
Santiago V. Salazar ◽  
Timothy O. Cox ◽  
Suho Lee ◽  
A. Harrison Brody ◽  
Annabel S. Chyung ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Factor ◽  
Disease Risk ◽  
Amyloid Β ◽  
Synaptic Dysfunction ◽  
Disease Risk Factor

scholarly journals Alzheimer’s disease risk factor mutations in patients diagnosed with Creutzfelt‐Jakob disease

2020 ◽  
Vol 16 (S3) ◽  
Author(s):  
Eva Bagyinszky ◽  
Lindsay A. Farrer ◽  
John Farrell ◽  
Giau Van Vo ◽  
KyuHwan Shim ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Factor ◽  
Disease Risk ◽  
Disease Risk Factor ◽  
Jakob Disease

scholarly journals PICALM Rescues Endocytic Defects Caused by the Alzheimer’s Disease Risk Factor APOE4

Cell Reports ◽  
2020 ◽  
Vol 33 (1) ◽  
pp. 108224
Author(s):  
Priyanka Narayan ◽  
Grzegorz Sienski ◽  
Julia M. Bonner ◽  
Yuan-Ta Lin ◽  
Jinsoo Seo ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Factor ◽  
Disease Risk ◽  
Disease Risk Factor

Alzheimer's disease risk factor complement receptor 1 is associated with depression

2012 ◽  
Vol 510 (1) ◽  
pp. 6-9 ◽  
Author(s):  
Gillian Hamilton ◽  
Kathryn L. Evans ◽  
Donald J. MacIntyre ◽  
Ian J. Deary ◽  
Anna Dominiczak ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Factor ◽  
Disease Risk ◽  
Complement Receptor ◽  
Disease Risk Factor ◽  
Complement Receptor 1

scholarly journals The Alzheimer's disease risk factor CD2AP maintains blood–brain barrier integrity

2015 ◽  
Vol 24 (23) ◽  
pp. 6667-6674 ◽  
Author(s):  
J. Nicholas Cochran ◽  
Travis Rush ◽  
Susan C. Buckingham ◽  
Erik D. Roberson
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Factor ◽  
Blood Brain Barrier ◽  
Disease Risk ◽  
Brain Barrier ◽  
Disease Risk Factor ◽  
Barrier Integrity ◽  
Blood Brain ◽  
Blood Brain Barrier Integrity

scholarly journals P4-517: EXPRESSION OF THE ALZHEIMER'S DISEASE RISK FACTOR SORLA IN THE POSTNATAL MOUSE RETINA

2019 ◽  
Vol 15 ◽  
pp. P1512-P1512
Author(s):  
Giulia Monti ◽  
Marianne Lundsgaard Kristensen ◽  
Arnela Mehmedbasic ◽  
Margarita Melnikova ◽  
Ida E. Holm ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Factor ◽  
Disease Risk ◽  
Mouse Retina ◽  
Disease Risk Factor

P1-087: Placental tau, α-synuclein, Aβ, and app levels in preeclampsia: An Alzheimer's disease risk factor

2015 ◽  
Vol 11 (7S_Part_8) ◽  
pp. P372-P372
Author(s):  
Edward G. Stopa ◽  
James Padbury ◽  
Lori A. Daiello ◽  
Brian R. Ott ◽  
Surendra Sharma
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Factor ◽  
Disease Risk ◽  
Disease Risk Factor

scholarly journals The Alzheimer’s disease risk factor APOE4 drives pro-inflammation in human astrocytes via HDAC-dependent repression of TAGLN3

2021 ◽  
Author(s):  
Laurie Arnaud ◽  
Philippe Benech ◽  
Louise Greetham ◽  
Delphine Stephan ◽  
Angélique Jimenez ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Factor ◽  
Transcriptional Repression ◽  
Inflammatory Responses ◽  
Disease Risk ◽  
Late Onset ◽  
Patient Specific ◽  
Potential Biomarker ◽  
Induced Pluripotent

ABSTRACTThe Apolipoprotein E4 (APOE4) is the major allelic risk factor for late-onset Alzheimer’s disease (AD). APOE4 associates with a pro-inflammatory phenotype increasingly considered as critical in AD initiation and progression. Yet, the mechanisms driving an APOE4-dependent neuroinflammation remain unelucidated. Leveraging patient specific human induced Pluripotent Stem Cells (iPSCs) we demonstrate inflammatory chronicity and hyperactivated responses upon cytokines in human APOE4 astrocytes via a novel mechanism. We uncovered that APOE4 represses Transgelin 3 (TAGLN3), a new interacting partner of IκBα, thus increasing the NF-kB activity. The transcriptional repression of TAGLN3 was shown to result from an APOE4-dependent histone deacetylase (HDAC) activity. The functional relevance of TAGLN3 was demonstrated by the attenuation of APOE4-driven neuroinflammation after TAGLN3 supplementation. Importantly, TAGLN3 downregulation was confirmed in the brain of AD patients. Our findings highlight the APOE4-TAGLN3 axis as a new pathogenic pathway that paves the way for the development of therapeutics to prevent maladaptive inflammatory responses in APOE4 carriers, while placing TAGLN3 downregulation as a potential biomarker of AD.GRAPHICAL ABSTRACT

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