Tau deposition and microglial activation in the living brain of early-stage Alzheimer disease

2017 ◽  
Vol 381 ◽  
pp. 127-128
Author(s):  
T. Terada ◽  
T. Bunai ◽  
T. Matsudaira ◽  
Y. Araki ◽  
A. Sugiura ◽  
...  

2011 ◽  
Vol 7 (8) ◽  
pp. 420-420 ◽  
Author(s):  
Katy Malpass


2011 ◽  
Vol 286 (37) ◽  
pp. 32713-32722 ◽  
Author(s):  
Seo-Hyun Cho ◽  
Binggui Sun ◽  
Yungui Zhou ◽  
Tiina M. Kauppinen ◽  
Brian Halabisky ◽  
...  


2016 ◽  
Vol 80 (2) ◽  
pp. 301-306 ◽  
Author(s):  
Jake G. Hoekstra ◽  
Michael J. Hipp ◽  
Thomas J. Montine ◽  
Scott R. Kennedy


Neurology ◽  
2018 ◽  
Vol 90 (22) ◽  
pp. e1989-e1996 ◽  
Author(s):  
Luca Passamonti ◽  
Patricia Vázquez Rodríguez ◽  
Young T. Hong ◽  
Kieren S.J. Allinson ◽  
W. Richard Bevan-Jones ◽  
...  

ObjectiveWe tested whether in vivo neuroinflammation relates to the distinctive distributions of pathology in Alzheimer disease (AD) and progressive supranuclear palsy (PSP).MethodsSixteen patients with symptomatic AD (including amnestic mild cognitive impairment with amyloid-positive PET scan), 16 patients with PSP–Richardson syndrome, and 13 age-, sex-, and education-matched healthy controls were included in this case-control study. Participants underwent [11C]PK11195 PET scanning, which was used as an in vivo index of neuroinflammation.Results[11C]PK11195 binding in the medial temporal lobe and occipital, temporal, and parietal cortices was increased in patients with AD, relative both to patients with PSP and to controls. Compared to controls, patients with PSP showed elevated [11C]PK11195 binding in the thalamus, putamen, and pallidum. [11C]PK11195 binding in the cuneus/precuneus correlated with episodic memory impairment in AD, while [11C]PK11195 binding in the pallidum, midbrain, and pons correlated with disease severity in PSP.ConclusionsTogether, our results suggest that neuroinflammation has an important pathogenic role in the 2 very different human neurodegenerative disorders of AD and PSP. The increase and distribution of microglial activation suggest that immunotherapeutic strategies may be useful in slowing the progression of both diseases.



Neurology ◽  
2020 ◽  
Vol 95 (16) ◽  
pp. e2259-e2270 ◽  
Author(s):  
Alice D. Lam ◽  
Rani A. Sarkis ◽  
Kyle R. Pellerin ◽  
Jin Jing ◽  
Barbara A. Dworetzky ◽  
...  

ObjectiveTo examine the relationship between scalp EEG biomarkers of hyperexcitability in Alzheimer disease (AD) and to determine how these electric biomarkers relate to the clinical expression of seizures in AD.MethodsIn this cross-sectional study, we performed 24-hour ambulatory scalp EEGs on 43 cognitively normal elderly healthy controls (HC), 41 participants with early-stage AD with no history or risk factors for epilepsy (AD-NoEp), and 15 participants with early-stage AD with late-onset epilepsy related to AD (AD-Ep). Two epileptologists blinded to diagnosis visually reviewed all EEGs and annotated all potential epileptiform abnormalities. A panel of 9 epileptologists blinded to diagnosis was then surveyed to generate a consensus interpretation of epileptiform abnormalities in each EEG.ResultsEpileptiform abnormalities were seen in 53% of AD-Ep, 22% of AD-NoEp, and 4.7% of HC. Specific features of epileptiform discharges, including high frequency, robust morphology, right temporal location, and occurrence during wakefulness and REM, were associated with clinical seizures in AD. Multiple EEG biomarkers concordantly demonstrated a pattern of left temporal lobe hyperexcitability in early stages of AD, whereas clinical seizures in AD were often associated with bitemporal hyperexcitability. Frequent small sharp spikes were specifically associated with epileptiform EEGs and thus identified as a potential biomarker of hyperexcitability in AD.ConclusionEpileptiform abnormalities are common in AD but not all equivalent. Specific features of epileptiform discharges are associated with clinical seizures in AD. Given the difficulty recognizing clinical seizures in AD, these EEG features could provide guidance on which patients with AD are at high risk for clinical seizures.



2012 ◽  
Vol 35 (2) ◽  
pp. 72-78 ◽  
Author(s):  
Eric D. Vidoni ◽  
Sandra A. Billinger ◽  
Charesa Lee ◽  
Jenna Hamilton ◽  
Jeffrey M. Burns


2019 ◽  
Vol 42 (3) ◽  
pp. E129-E134 ◽  
Author(s):  
Eric D. Vidoni ◽  
Jaime Perales ◽  
Mohammed Alshehri ◽  
Abdul-Mannaan Giles ◽  
Catherine F. Siengsukon ◽  
...  


2008 ◽  
Vol 202 (1-3) ◽  
pp. 37-51 ◽  
Author(s):  
Evelin L. Schaeffer ◽  
Orestes V. Forlenza ◽  
Wagner F. Gattaz




2014 ◽  
Vol 10 ◽  
pp. P616-P617
Author(s):  
Yumi Umeda-Kameyama ◽  
Katsuya Iijima ◽  
Kiyoshi Yamaguchi ◽  
Kiwami Kidana ◽  
Masayuki Honda ◽  
...  


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