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Keywords: Alzheimer's disease
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Journal Articles
J Cell Sci (2022) 135 (12): jcs259764.
Published: 21 June 2022
..., many are now entering the prime age when Alzheimer's disease (AD)-like symptoms begin to manifest. It has been shown that hyperphosphorylated tau, a known AD pathological characteristic, is prematurely increased in the brains of HIV-infected individuals as early as in their 30s and that its levels...
Includes: Supplementary data
Journal Articles
J Cell Sci (2022) 135 (2): jcs258687.
Published: 25 January 2022
...Gianna M. Fote; Nicolette R. Geller; Nikolaos E. Efstathiou; Nathan Hendricks; Demetrios G. Vavvas; Jack C. Reidling; Leslie M. Thompson; Joan S. Steffan ABSTRACT The human apolipoprotein E4 isoform (APOE4) is the strongest genetic risk factor for late-onset Alzheimer's disease (AD), and lysosomal...
Includes: Supplementary data
Journal Articles
J Cell Sci (2021) 134 (20): jcs258894.
Published: 21 October 2021
...., 2012 ). ApoE also bears significance as the most important genetic risk factor for the sporadic form of Alzheimer's disease (AD) as carriers of the APOEε4 allele (encoding apoE4) are at a significantly higher risk of developing AD than individuals having the common APOEε3 gene variant (encoding...
Includes: Supplementary data
Journal Articles
J Cell Sci (2021) 134 (8): jcs254904.
Published: 22 April 2021
..., contributing to the pathophysiology of Alzheimer's disease. In this Review, we discuss the principles of the ‘nuclear calcium hypothesis’ in the context of human brain function and its role in controlling diverse forms of neuroadaptation and neuroprotection. Furthermore, we present the most relevant...
Journal Articles
J Cell Sci (2020) 133 (23): jcs243139.
Published: 11 December 2020
...Natasha Vassileff; Lesley Cheng; Andrew F. Hill ABSTRACT Neurodegenerative diseases are characterised by the irreversible degeneration of neurons in the central or peripheral nervous systems. These include amyotrophic lateral sclerosis (ALS), Alzheimer's disease (AD), Parkinson's disease (PD...
Includes: Supplementary data
Journal Articles
J Cell Sci (2020) 133 (7): jcs239756.
Published: 8 April 2020
... the characterization of mRNAs encoding GFAP-α and GFAP-δ isoforms as a proof of concept, we showed that they mainly localized on GFAP processes. In the APPswe/PS1dE9 mouse model of Alzheimer's disease, the density and distribution of both α and δ forms of Gfap mRNA changed as a function of the region...
Includes: Supplementary data
Journal Articles
J Cell Sci (2020) 133 (5): jcs238030.
Published: 10 January 2020
... that dual inhibition of the SHIP1 and 2 paralogs can provide a novel means to enhance basal microglial homeostatic functions for therapeutic purposes in Alzheimer's disease and, possibly, other types of dementia where increased microglial function could be beneficial. * These authors contributed...
Includes: Supplementary data
Journal Articles
J Cell Sci (2019) 132 (14): jcs229054.
Published: 15 July 2019
... hippocampal cultures and adult mouse brain. Finally, SHP2 levels were upregulated in samples from patients with mild and severe Alzheimer's disease (AD), and the level of tau–SHP2 complexes were increased in AD patient samples. These findings strongly suggest a role for the tau–SHP2 interaction in NGF...
Includes: Supplementary data
Journal Articles
J Cell Sci (2019) 132 (13): jcs231258.
Published: 1 July 2019
...Dina S. Coelho; Eduardo Moreno ABSTRACT Alzheimer's disease (AD) causes a progressive loss of memory and other cognitive functions, which inexorably debilitates patients. There is still no cure for AD and effective treatments to delay or revert AD are urgently needed. On a molecular level...
Journal Articles
In collection:
Mitochondria
J Cell Sci (2017) 130 (18): 3023–3039.
Published: 15 September 2017
...Kumar Nikhil; Kavita Shah ABSTRACT Cdk5 deregulation is highly neurotoxic in Alzheimer's disease (AD). We identified Mcl-1 as a direct Cdk5 substrate using an innovative chemical screen in mouse brain lysates. Our data demonstrate that Mcl-1 levels determine the threshold for cellular damage...
Includes: Supplementary data
Journal Articles
J Cell Sci (2016) 129 (11): 2224–2238.
Published: 1 June 2016
... ABSTRACT Dysfunction and loss of synapses are early pathogenic events in Alzheimer's disease. A central step in the generation of toxic amyloid-β (Aβ) peptides is the cleavage of amyloid precursor protein (APP) by β-site APP-cleaving enzyme (BACE1). Here, we have elucidated whether downregulation of septin...
Includes: Supplementary data
Journal Articles
J Cell Sci (2016) 129 (10): 2003–2015.
Published: 15 May 2016
...Xu Yan; Niko-Petteri Nykänen; Cecilia A. Brunello; Annakaisa Haapasalo; Mikko Hiltunen; Riikka-Liisa Uronen; Henri J. Huttunen ABSTRACT One of the defining pathological features of Alzheimer's disease is the intraneuronal accumulation of tau (also known as MAPT) protein. Tau is also secreted from...
Journal Articles
J Cell Sci (2016) 129 (9): 1815–1830.
Published: 1 May 2016
...Chun Shi; Keith Viccaro; Hyoung-gon Lee; Kavita Shah ABSTRACT Deregulated Cdk5 causes neurotoxic amyloid beta peptide (Aβ) processing and cell death, two hallmarks of Alzheimer's disease, through the Foxo3 transcriptional factor in hippocampal cells, primary neurons and an Alzheimer's disease mouse...
Journal Articles
In collection:
Membrane Trafficking
J Cell Sci (2015) 128 (14): 2520–2528.
Published: 15 July 2015
...James R. Edgar; Katarina Willén; Gunnar K. Gouras; Clare E. Futter ABSTRACT Intracellular amyloid-β (Aβ) accumulation is a key feature of early Alzheimer's disease and precedes the appearance of Aβ in extracellular plaques. Aβ is generated through proteolytic processing of amyloid precursor protein...
Includes: Supplementary data
Journal Articles
J Cell Sci (2015) 128 (13): 2330–2338.
Published: 1 July 2015
...Valérie Vingtdeux; Pallavi Chandakkar; Haitian Zhao; Lionel Blanc; Santiago Ruiz; Philippe Marambaud ABSTRACT Alzheimer's disease is characterized by amyloid-β (Aβ) peptide accumulation in the brain. CALHM1, a cell-surface Ca 2+ channel expressed in brain neurons, has anti-amyloidogenic properties...
Journal Articles
J Cell Sci (2015) 128 (7): 1259–1267.
Published: 1 April 2015
... defective autophagy in neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS), Alzheimer's disease, Parkinson's disease and Huntington's disease. Recent work using live-cell imaging has identified autophagy as a predominantly polarized process in neuronal axons; autophagosomes...
Includes: Supplementary data
Journal Articles
J Cell Sci (2014) 127 (11): 2391–2400.
Published: 1 June 2014
... neuronal processes, including higher cognitive functions such as learning and memory formation. However, Cdk5 activity becomes deregulated in several neurological disorders, such as Alzheimer's disease, Parkinson's disease and Huntington's disease, which leads to neurotoxicity. Therefore, precise control...
Journal Articles
J Cell Sci (2013) 126 (18): 4136–4146.
Published: 15 September 2013
... of Alzheimer's disease. Taken together, our findings indicate that UPR genes are critical for maintaining secretory protein metabolism under normal growth conditions. Funding This study was supported by the National Institutes of Health [grant number R37 AG011816 to C.K.]; the United States–Israel...
Includes: Supplementary data
Journal Articles
J Cell Sci (2013) 126 (9): 2079–2091.
Published: 1 May 2013
... are segregated, with tau being mainly localised to the axon and MAP2 mainly to the dendrite. In particular, tau plays a crucial role in pathology, as elevated levels lead to the formation of tau aggregates in many neurodegenerative conditions including Alzheimer's disease. We used PTL-1 in C. elegans to model...
Includes: Supplementary data
Journal Articles
J Cell Sci (2013) 126 (5): 1199–1206.
Published: 1 March 2013
...Ute Dreses-Werringloer; Valérie Vingtdeux; Haitian Zhao; Pallavi Chandakkar; Peter Davies; Philippe Marambaud Summary Calcium homeostasis modulator 1 (CALHM1) is a Ca 2+ channel controlling neuronal excitability and potentially involved in the pathogenesis of Alzheimer's disease (AD). Although...