scholarly journals Earlier age at onset for APOE e4-mediated β-amyloid deposition in East Asians

IBRO Reports ◽  
2019 ◽  
Vol 6 ◽  
pp. S454-S455
Author(s):  
Tamil Iniyan Gunasekaran ◽  
Jang Jae Lee ◽  
Yu Yong Choi ◽  
Sarang Kang ◽  
Jungsoo Gim ◽  
...  
2020 ◽  
Vol 20 (9) ◽  
pp. 770-781 ◽  
Author(s):  
Poornima Sharma ◽  
Anjali Sharma ◽  
Faizana Fayaz ◽  
Sharad Wakode ◽  
Faheem H. Pottoo

Alzheimer’s disease (AD) is the most prevalent and severe neurodegenerative disease affecting more than 0.024 billion people globally, more common in women as compared to men. Senile plaques and amyloid deposition are among the main causes of AD. Amyloid deposition is considered as a central event which induces the link between the production of β amyloid and vascular changes. Presence of numerous biomarkers such as cerebral amyloid angiopathy, microvascular changes, senile plaques, changes in white matter, granulovascular degeneration specifies the manifestation of AD while an aggregation of tau protein is considered as a primary marker of AD. Likewise, microvascular changes, activation of microglia (immune defense system of CNS), amyloid-beta aggregation, senile plaque and many more biomarkers are nearly found in all Alzheimer’s patients. It was seen that 70% of Alzheimer’s cases occur due to genetic factors. It has been reported in various studies that apolipoprotein E(APOE) mainly APOE4 is one of the major risk factors for the later onset of AD. Several pathological changes also occur in the white matter which include dilation of the perivascular space, loss of axons, reactive astrocytosis, oligodendrocytes and failure to drain interstitial fluid. In this review, we aim to highlight the various biological signatures associated with the AD which may further help in discovering multitargeting drug therapy.


2008 ◽  
Vol 67 (2) ◽  
pp. 155-161 ◽  
Author(s):  
Michail E. Kalaitzakis ◽  
Manuel B. Graeber ◽  
Stephen M. Gentleman ◽  
Ronald K. B. Pearce

2022 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Dongyu Fan ◽  
Huiyun Li ◽  
Dongwan Chen ◽  
Yang Chen ◽  
Xu Yi ◽  
...  

2013 ◽  
Vol 72 (4) ◽  
pp. 272-285 ◽  
Author(s):  
Juan Jose Ramos-Rodriguez ◽  
Mar Pacheco-Herrero ◽  
Diana Thyssen ◽  
Maria Isabel Murillo-Carretero ◽  
Esther Berrocoso ◽  
...  

2010 ◽  
Vol 6 ◽  
pp. S235-S235
Author(s):  
Hiroshige Fujishiro ◽  
Eizo Iseki ◽  
Shinji Higashi ◽  
Koji Kasanuki ◽  
Ryoko Yamamoto ◽  
...  

2020 ◽  
Vol 77 (3) ◽  
pp. 350 ◽  
Author(s):  
Rebecca F. Gottesman ◽  
Thomas H. Mosley ◽  
David S. Knopman ◽  
Qing Hao ◽  
Dean Wong ◽  
...  

Author(s):  
S. Tolbert ◽  
Y. Liu ◽  
C. Hellegers ◽  
J.R. Petrella ◽  
M.W. Weiner ◽  
...  

Background: There is a need to more fully characterize financial capacity losses in the preclinical and prodromal stages of Alzheimer’s disease (AD) and their pathological substrates. Objectives: To test the association between financial skills and cortical β-amyloid deposition in aging and subjects at risk for AD. Design: Cross-sectional analyses of data from the Alzheimer’s Disease Neuroimaging Initiative (ADNI-3) study conducted across 50 plus sites in the US and Canada. Setting: Multicenter biomarker study. Participants: 243 subjects (144 cognitively normal, 79 mild cognitive impairment [MCI], 20 mild AD). Measurements: 18F-Florbetapir brain PET scans to measure global cortical β-amyloid deposition (SUVr) and the Financial Capacity Instrument Short Form (FCI-SF) to evaluate an individual’s financial skills in monetary calculation, financial concepts, checkbook/register usage, and bank statement usage. There are five sub scores and a total score (range of 0–74) with higher scores indicating better financial skill. Results: FCI-SF total score was significantly worse in MCI [Cohen’s d= 0.9 (95%CI: 0.6-1.2)] and AD subjects [Cohen’s d=3.1(CI: 2.5-3.7)] compared to normals. Domain scores and completion times also showed significant difference. Across all subjects, higher cortical β-amyloid SUVr was significantly associated with worse FCI-SF total score after co-varying for age, education, and cognitive score [Cohen’s f2=0.751(CI: 0.5-1.1)]. In cognitively normal subjects, after covarying for age, gender, and education, higher β -amyloid PET SUVr was associated with longer task completion time [Cohen’s f2=0.198(CI: 0.06-0.37)]. Conclusion: Using a multicenter study sample, we document that financial capacity is impaired in the prodromal and mild stages of AD and that such impairments are, in part, associated with the extent of cortical β-amyloid deposition. In normal aging, β-amyloid deposition is associated with slowing of financial tasks. These data confirm and extend prior research highlighting the utility of financial capacity assessments in at risk samples.


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