scholarly journals Modeling the Relationships Among Late-Life Body Mass Index, Cerebrovascular Disease, and Alzheimer’s Disease Neuropathology in an Autopsy Sample of 1,421 Subjects from the National Alzheimer’s Coordinating Center Data Set

2017 ◽  
Vol 57 (3) ◽  
pp. 953-968 ◽  
Author(s):  
Michael L. Alosco ◽  
Jonathan Duskin ◽  
Lilah M. Besser ◽  
Brett Martin ◽  
Christine E. Chaisson ◽  
...  
Author(s):  
Jena N Moody ◽  
, Kate E Valerio ◽  
M S, Alexander N Hasselbach ◽  
Sarah Prieto ◽  
M S, Mark W Logue ◽  
...  

Abstract Body mass index (BMI) is a risk factor for Alzheimer’s disease (AD) although the relationship is complex. Obesity in midlife is associated with increased risk for AD, whereas evidence supports both higher and lower BMI increasing risk for AD in late life. This study examined the influence of individual differences in genetic risk for AD to further clarify the relationship between late-life BMI and conversion to AD. Participants included 52 individuals diagnosed as having mild cognitive impairment (MCI) at baseline who converted to AD within 24 months and 52 matched MCI participants from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) cohort. BMI was measured at baseline. Genetic risk for AD was assessed via genome-wide polygenic risk scores. Conditional logistic regression models were run to determine if BMI and polygenic risk predicted conversion to AD. Results showed an interaction between BMI and genetic risk, such that individuals with lower BMI and higher polygenic risk were more likely to convert to AD relative to individuals with higher BMI. These results remained significant after adjusting for cerebrospinal fluid biomarkers of AD. Exploratory sex-stratified analyses revealed this relationship only remained significant in males. These results show that higher genetic risk in the context of lower BMI predicts conversion to AD in the next 24 months, particularly among males. These findings suggest that genetic risk for AD in the context of lower BMI may serve as a prodromal risk factor for future conversion to AD.


2020 ◽  
Vol 17 (2) ◽  
pp. 185-195
Author(s):  
Jianxiong Xi ◽  
Ding Ding ◽  
Qianhua Zhao ◽  
Xiaoniu Liang ◽  
Li Zheng ◽  
...  

Background: Approximately 40 independent Single Nucleotide Polymorphisms (SNPs) have been associated with Alzheimer’s Disease (AD) or cognitive decline in genome-wide association studies. Methods: We aimed to evaluate the joint effect of genetic polymorphisms and environmental factors on the progression from Mild Cognitive Impairment (MCI) to AD (MCI-AD progression) in a Chinese community cohort. Conclusion: Demographic, DNA and incident AD diagnosis data were derived from the follow-up of 316 participants with MCI at baseline of the Shanghai Aging Study. The associations of 40 SNPs and environmental predictors with MCI-AD progression were assessed using the Kaplan-Meier method with the log-rank test and Cox regression model. Results: Rs4147929 at ATP-binding cassette family A member 7 (ABCA7) (AG/AA vs. GG, hazard ratio [HR] = 2.43, 95% confidence interval [CI] 1.24-4.76) and body mass index (BMI) (overweight vs. non-overweight, HR = 0.41, 95% CI 0.22-0.78) were independent predictors of MCI-AD progression. In the combined analyses, MCI participants with the copresence of non-overweight BMI and the ABCA7 rs4147929 (AG/AA) risk genotype had an approximately 6-fold higher risk of MCI-AD progression than those with an overweight BMI and a non-risk genotype (HR = 6.77, 95% CI 2.60-17.63). However, a nonsignificant result was found when participants carried only one of these two risk factors (nonoverweight BMI and AG/AA of ABCA7 rs4147929). Conclusion: ABCA7 rs4147929 and BMI jointly affect MCI-AD progression. MCI participants with the rs4147929 risk genotype may benefit from maintaining an overweight BMI level with regard to their risk for incident AD.


2015 ◽  
Vol 36 ◽  
pp. S194-S202 ◽  
Author(s):  
Christina P. Boyle ◽  
Cyrus A. Raji ◽  
Kirk I. Erickson ◽  
Oscar L. Lopez ◽  
James T. Becker ◽  
...  

2020 ◽  
Vol 25 ◽  
pp. 102156
Author(s):  
Jasmeet P. Hayes ◽  
Jena N. Moody ◽  
Juan Guzmán Roca ◽  
Scott M. Hayes

2000 ◽  
Vol 12 (1) ◽  
pp. 87-98 ◽  
Author(s):  
Michel Bédard ◽  
D. William Molloy ◽  
Rhonda Bell ◽  
Judy A. Lever

Objective: To determine the proportion of older adults with Alzheimer's disease presenting to a geriatric clinic with low body mass index (BMI), the proportion of these individuals recognized by clinicians as malnourished, and what patients' characteristics and caregivers' and clinicians' impressions are associated with low BMI. Design: Cross-sectional study. Setting: An outpatient geriatric clinic located in a university-affiliated teaching hospital. Participants: 340 patients with Alzheimer's disease, average age 75 years. Measurements: Individuals with a BMI below 21 were considered at risk of malnutrition. Physical examination and medical information were obtained from patients and caregivers by clinicians using a standardized assessment protocol. Clinicians' impression regarding evidence of malnutrition was obtained. Results: Forty-six patients (16%) had a BMI below 21. Clinicians reported evidence of potential malnutrition in 11 patients, 8 of whom had a BMI below 21. Using logistic regression, we found that women were five times more likely to have a BMI below 21 than men, and that individuals with low cognition were twice as likely to have a BMI below 21 than individuals with higher cognition. Conclusion: The proportion of patients with Alzheimer's disease with a BMI below 21 is similar to that encountered in the general population aged 65+. However, clinicians have difficulty identifying persons at risk of malnutrition according to BMI status. Women with low cognition were at increased risk of having a low BMI. Improvement in the detection of malnutrition is desirable. Further exploration of causal links between cognition and malnutrition is required.


2015 ◽  
Vol 11 (12) ◽  
pp. 1439-1451 ◽  
Author(s):  
Shubhabrata Mukherjee ◽  
Stefan Walter ◽  
John S.K. Kauwe ◽  
Andrew J. Saykin ◽  
David A. Bennett ◽  
...  

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