scholarly journals Distinct Chronology of Neuronal Cell Cycle Re-Entry and Tau Pathology in the 3xTg-AD Mouse Model and Alzheimer's Disease Patients

2014 ◽  
Vol 43 (1) ◽  
pp. 57-65 ◽  
Author(s):  
Alex C. Hradek ◽  
Hyun-Pil Lee ◽  
Sandra L. Siedlak ◽  
Sandy L. Torres ◽  
Wooyoung Jung ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Cell Cycle ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Neuronal Cell ◽  
Tau Pathology ◽  
Ad Mouse Model

scholarly journals Microglial derived tumor necrosis factor-α drives Alzheimer's disease-related neuronal cell cycle events

2014 ◽  
Vol 62 ◽  
pp. 273-285 ◽  
Author(s):  
Kiran Bhaskar ◽  
Nicole Maphis ◽  
Guixiang Xu ◽  
Nicholas H. Varvel ◽  
Olga N. Kokiko-Cochran ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Cell Cycle ◽  
Alzheimer's Disease ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Neuronal Cell ◽  
Factor Α ◽  
Necrosis Factor

S5-01-01: The pathway from amyloid to tau for aberrant neuronal cell cycle re-entry in Alzheimer's disease

2012 ◽  
Vol 8 (4S_Part_20) ◽  
pp. P724-P724
Author(s):  
Matthew Seward ◽  
Eric Swanson ◽  
Erik Roberson ◽  
George Bloom
Keyword(s):  
Alzheimer’S Disease ◽  
Cell Cycle ◽  
Alzheimer's Disease ◽  
Neuronal Cell

scholarly journals Reduced non–rapid eye movement sleep is associated with tau pathology in early Alzheimer’s disease

2019 ◽  
Vol 11 (474) ◽  
pp. eaau6550 ◽  
Author(s):  
Brendan P. Lucey ◽  
Austin McCullough ◽  
Eric C. Landsness ◽  
Cristina D. Toedebusch ◽  
Jennifer S. McLeland ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Eye Movement ◽  
Single Channel ◽  
Amyloid Β ◽  
Neuronal Cell ◽  
Rapid Eye Movement ◽  
Tau Pathology ◽  
Potential Marker

In Alzheimer’s disease (AD), deposition of insoluble amyloid-β (Aβ) is followed by intracellular aggregation of tau in the neocortex and subsequent neuronal cell loss, synaptic loss, brain atrophy, and cognitive impairment. By the time even the earliest clinical symptoms are detectable, Aβ accumulation is close to reaching its peak and neocortical tau pathology is frequently already present. The period in which AD pathology is accumulating in the absence of cognitive symptoms represents a clinically relevant time window for therapeutic intervention. Sleep is increasingly recognized as a potential marker for AD pathology and future risk of cognitive impairment. Previous studies in animal models and humans have associated decreased non–rapid eye movement (NREM) sleep slow wave activity (SWA) with Aβ deposition. In this study, we analyzed cognitive performance, brain imaging, and cerebrospinal fluid (CSF) AD biomarkers in participants enrolled in longitudinal studies of aging. In addition, we monitored their sleep using a single-channel electroencephalography (EEG) device worn on the forehead. After adjusting for multiple covariates such as age and sex, we found that NREM SWA showed an inverse relationship with AD pathology, particularly tauopathy, and that this association was most evident at the lowest frequencies of NREM SWA. Given that our study participants were predominantly cognitively normal, this suggested that changes in NREM SWA, especially at 1 to 2 Hz, might be able to discriminate tau pathology and cognitive impairment either before or at the earliest stages of symptomatic AD.

scholarly journals Transient Cerebral Ischemia Induces Aberrant Neuronal Cell Cycle Re-entry and Alzheimer's Disease-like Tauopathy in Female Rats

2004 ◽  
Vol 279 (21) ◽  
pp. 22684-22692 ◽  
Author(s):  
Yi Wen ◽  
Shaohua Yang ◽  
Ran Liu ◽  
Anne Marie Brun-Zinkernagel ◽  
Peter Koulen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Cell Cycle ◽  
Alzheimer's Disease ◽  
Cerebral Ischemia ◽  
Neuronal Cell ◽  
Transient Cerebral Ischemia ◽  
Female Rats
Sign in / Sign up

Export Citation Format

Share Document