scholarly journals Amyloid Burden in Alzheimer's Disease Patients Is Associated with Alterations in Circadian Rhythm

2021 ◽  
Vol 20 (4) ◽  
pp. 99
Author(s):  
Jubin Kang ◽  
Hyung Jin Choi ◽  
Gary D. Isaacs ◽  
Wonjae Sung ◽  
Hee-Jin Kim
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Circadian Rhythm ◽  
Amyloid Burden

Circadian Rhythm Disturbance in Agitation of Alzheimer's Disease

2021 ◽  
Vol 29 (4) ◽  
pp. S111-S113
Author(s):  
John Outen ◽  
Adam Spira ◽  
Sarah Wanigatunga ◽  
Vadim Zipunnikov ◽  
Mark Wu ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Circadian Rhythm ◽  
Rhythm Disturbance

scholarly journals Unique Sleep and Circadian Rhythm Dysfunction Neuroinflammatory and Immune Profiles in Alzheimer’s Disease with Mild Cognitive Impairment

2021 ◽  
pp. 1-6
Author(s):  
Jagan A. Pillai ◽  
James Bena ◽  
Lynn M. Bekris ◽  
Nancy Foldvary-Schaefer ◽  
Catherine Heinzinger ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebrospinal Fluid ◽  
Circadian Rhythm ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Humoral Immune ◽  
Humoral Immune Responses ◽  
Cerebrospinal Fluid Biomarkers ◽  
Circulating Markers

Sleep dysfunction has been identified in the pathophysiology of Alzheimer’s disease (AD); however, the role and mechanism of circadian rhythm dysfunction is less well understood. In a well-characterized cohort of patients with AD at the mild cognitive impairment stage (MCI-AD), we identify that circadian rhythm irregularities were accompanied by altered humoral immune responses detected in both the cerebrospinal fluid and plasma as well as alterations of cerebrospinal fluid biomarkers of neurodegeneration. On the other hand, sleep disruption was more so associated with abnormalities in circulating markers of immunity and inflammation and decrements in cognition.

24 hour cortisol circadian rhythm in Alzheimer's disease: Comparison with normal subjects

1994 ◽  
Vol 15 ◽  
pp. S10
Author(s):  
C.E. Rosenberg ◽  
J. Lee ◽  
D. Rowland ◽  
P.J. Whitehouse
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Circadian Rhythm ◽  
Normal Subjects

scholarly journals P3-270: CHF5074 reduces brain β-amyloid burden and hyperphosphorylated tau in a mouse model of Alzheimer's disease

2009 ◽  
Vol 5 (4S_Part_14) ◽  
pp. P422-P422
Author(s):  
M. Pizzi ◽  
A. Lanzillotta ◽  
B.P. Imbimbo ◽  
B. Hutter-Paier ◽  
G. Villetti ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Hyperphosphorylated Tau ◽  
Amyloid Burden ◽  
Model Of Alzheimer’S Disease ◽  
Β Amyloid

P4-140: AMYLOID BURDEN-RELATED PERFORMANCE DIFFERENCES ON COGNITIVE AND FUNCTIONAL INSTRUMENTS ACROSS ALZHEIMER'S DISEASE PATHOPHYSIOLOGIC STAGES

2014 ◽  
Vol 10 ◽  
pp. P839-P839
Author(s):  
Richard Margolin ◽  
Jianing Di ◽  
Randolph Andrews ◽  
Stephen Salloway ◽  
Reisa Sperling ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Burden ◽  
Performance Differences

VANUTIDE CRIDIFICAR (ACC-001) AND QS-21 ADJUVANT IN INDIVIDUALS WITH EARLY ALZHEIMER’S DISEASE: AMYLOID IMAGING POSITRON EMISSION TOMOGRAPHY AND SAFETY RESULTS FROM A PHASE 2 STUDY

2016 ◽  
pp. 1-10
Author(s):  
C.H. van Dyck ◽  
C. Sadowsky ◽  
G. Le Prince Leterme ◽  
K. Booth ◽  
Y. Peng ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Positron Emission Tomography ◽  
Amyloid Beta ◽  
Standard Uptake Value ◽  
Emission Tomography ◽  
Amyloid Burden ◽  
Treatment Groups ◽  
Positron Emission ◽  
Early Alzheimer’S Disease

BACKGROUNDd: ACC-001 is an investigational therapeutic vaccine designed to elicit antibodies against the N-terminal peptide 1-7 of the amyloid-beta peptide, believed to be important in the pathogenesis of Alzheimer’s disease. OBJECTIVES: To evaluate safety, immunogenicity, impact on brain amyloid, and other exploratory endpoints in participants receiving ACC-001. DESIGN: Randomized, phase 2, interventional study. Trial registration: Clinicaltrials.gov ID NCT01227564. PARTICIPANTS: Individuals with early Alzheimer’s disease (Mini-Mental State Examination scores ≥25, a global Clinical Dementia Rating of 0.5, and evidence of elevated baseline brain amyloid burden). Intervention: Participants were randomized to ACC-001 3 µg or 10 µg with QS-21 adjuvant (50 µg), or placebo. MEASUREMENTS: The primary endpoint was change in brain amyloid burden by 18F-florbetapir positron emission tomography in composite cortical standard uptake value ratio. RESULTS: A total of 63 participants were randomized and 51 completed the study. At week 104, no significant differences were observed in 18F-florbetapir positron emission tomography composite cortical standard uptake value ratio between either ACC-001 dose compared with placebo. In both ACC-001 + QS-21 treatment groups, following the initial immunization, the anti-amyloid-beta geometric mean titers increased after each subsequent vaccination and then declined, with less apparent decline after the later compared with earlier immunizations. The majority of treatment-emergent adverse events in the ACC-001 + QS-21 groups were injection site reactions, which occurred at a greater rate in active treatment groups than in the placebo group. No amyloid-related imaging abnormalities of edema or effusion were reported. CONCLUSION: No statistically significant differences were observed between groups in the change from baseline brain amyloid burden despite apparently robust systemically measured anti-amyloid-beta antibody response at both dose levels. Insufficient antibody titers, poor quality immune response, short duration of treatment, or small sample size may have resulted in these findings. The safety and tolerability profile was acceptable.

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