scholarly journals Lewy body pathology in Alzheimer's disease: A clinicopathological prospective study

2018 ◽  
Vol 139 (1) ◽  
pp. 76-81 ◽  
Author(s):  
Rodolfo Savica ◽  
Thomas G. Beach ◽  
Joseph G. Hentz ◽  
Marwan N. Sabbagh ◽  
Geidy E. Serrano ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Prospective Study ◽  
Lewy Body ◽  
Lewy Body Pathology

Linkage of Parkinsonism and Alzheimer's disease with Lewy body pathology to chromosome 12

2002 ◽  
Vol 52 (4) ◽  
pp. 524-524
Author(s):  
William K. Scott ◽  
Jeffery M. Vance ◽  
Jonathan L. Haines ◽  
Margaret A. Pericak-Vance
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Lewy Body ◽  
Chromosome 12 ◽  
Lewy Body Pathology

Lewy body pathology is a frequent co-pathology in familial Alzheimer's disease

2003 ◽  
Vol 105 (5) ◽  
pp. 484-488 ◽  
Author(s):  
Yuri Trembath ◽  
Carolyn Rosenberg ◽  
John F. Ervin ◽  
Donald E. Schmechel ◽  
Perry Gaskell ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Lewy Body ◽  
Familial Alzheimer’S Disease ◽  
Lewy Body Pathology ◽  
Familial Alzheimer's Disease

scholarly journals Abnormal Sleep Behaviours Across the Spectrum of Alzheimer’s Disease Severity: Influence of APOE Genotypes and Lewy Bodies

2019 ◽  
Vol 16 (3) ◽  
pp. 243-250 ◽  
Author(s):  
Ka Yi G. Koo ◽  
Tom A. Schweizer ◽  
Corinne E. Fischer ◽  
David G. Munoz
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Lewy Body ◽  
Sleep Disturbances ◽  
Braak Stage ◽  
Sleep Patterns ◽  
Apoe Ε4 ◽  
Lewy Body Pathology ◽  
The Relationship ◽  
Abnormal Sleep

Background: The Apolipoprotein (APOE) ε4 allele is a well-known risk factor for Alzheimer’s Disease (AD), and sleep disturbances are commonly associated with AD. However, few studies have investigated the relationship between APOE ε4 and abnormal sleep patterns (N+) in AD. Objective: To examine the relationship between APOE genotype, Lewy body pathology, and abnormal sleep patterns in a large group of subjects with known AD load evaluated upon autopsy. Method: Data from 2,368 cases obtained from the National Alzheimer’s Coordinating Centre database were categorized as follows: Braak Stage V/VI and CERAD frequent neuritic plaques as high load AD, Braak Stage III/IV and moderate CERAD as intermediate load AD, and Braak Stage 0/I/II and infrequent CERAD as no to low load AD. Cases discrepant between the two measures were discarded. Results: Disrupted sleep was more frequent in males (42.4%) compared to females (35.1%), and in carriers (42.3%) as opposed to non-carriers (36.5%) of ε4. Amongst female subjects with high AD load and Lewy body pathology, homozygous (ε4/ε4) carriers experienced disrupted sleep more often compared with heterozygous (ε4/x) or non-carriers of ε4. Such recessive, gender-specific, and Lewy body association is reminiscent of the ε4 effect on psychosis in AD. However, such association was lost after adjusting for covariates. In subjects with no to low AD pathology, female ε4 carriers had significantly more nighttime disturbances than non-carriers; this effect is independent of the presence of Lewy body pathology. Conclusion: The influence of APOE ε4 on sleep disturbances is dependent on gender and severity of AD load.

Predicting Lewy Body Pathology in a Community-Based Sample With Clinical Diagnosis of Alzheimer’s Disease

2006 ◽  
Vol 19 (4) ◽  
pp. 195-201 ◽  
Author(s):  
Debby Tsuang ◽  
Kate Simpson ◽  
Eric B. Larson ◽  
Elaine Peskind ◽  
Walter Kukull ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Clinical Diagnosis ◽  
Lewy Body ◽  
Community Based ◽  
Lewy Body Pathology

scholarly journals The genetic contributions of SNCA and LRRK2 genes to Lewy Body pathology in Alzheimer's disease

2014 ◽  
Vol 23 (18) ◽  
pp. 4814-4821 ◽  
Author(s):  
C. Linnertz ◽  
M. W. Lutz ◽  
J. F. Ervin ◽  
J. Allen ◽  
N. R. Miller ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Lewy Body ◽  
Lewy Body Pathology ◽  
Genetic Contributions

scholarly journals Susceptibility to postmortem (co)-pathologies in antemortem atrophy-based subtypes of Alzheimer’s disease

2021 ◽  
Author(s):  
Rosaleena Mohanty ◽  
Daniel Ferreira ◽  
Simon Frerich ◽  
J-Sebastian Muehlboeck ◽  
Michel Grothe ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Lewy Body ◽  
Lewy Bodies ◽  
Alpha Synuclein ◽  
Magnetic Resonance Imaging Scan ◽  
Linear Regression Models ◽  
Lewy Body Pathology ◽  
Hippocampal Sparing ◽  
Regional Associations

AbstractObjectivesTo investigate whether antemortem atrophy-based subtypes of Alzheimer’s disease (AD) may be differentially susceptible to individual or concomitance of AD and non-AD (co)-pathologies, assessed neuropathologically at postmortem.MethodsWe selected 31 individuals from the AD neuroimaging initiative with: an antemortem magnetic resonance imaging scan evaluating brain atrophy available within two years before death; an antemortem diagnosis of AD dementia or prodromal AD; and postmortem neuropathological confirmation of AD. Antemortem atrophy-based subtypes was modeled as a continuous phenomenon in terms of two recently proposed dimensions: typicality (ranging from limbic-predominant AD to hippocampal-sparing AD subtypes) and severity (ranging from typical AD to minimal atrophy AD subtypes). Postmortem neuropathological evaluation included global and regional outcomes: AD hallmark pathologies of amyloid-beta and tau; non-AD co-pathologies of alpha-synuclein Lewy body and TDP-43; and the overall concomitance across these four (co)-pathologies. Partial correlation and linear regression models were used to assess the association between antemortem atrophy-based subtypes and postmortem neuropathological outcomes.ResultsWe observed significant global and regional associations between antemortem typicality and postmortem (co)-pathologies including tau, alpha-synuclein Lewy bodies and TDP-43. Antemortem typicality demonstrated stronger regional associations with concomitance of multiple postmortem (co)-pathologies in comparison to antemortem severity. Our findings suggest the following susceptibilities of atrophy-based subtypes: limbic-predominant AD towards higher burden of tau and TDP-43 pathologies while hippocampal-sparing AD towards lower burdens; limbic-predominant AD and typical AD towards higher burden of alpha-synuclein Lewy body pathology while hippocampal-sparing AD and minimal-atrophy AD towards lower burdens.DiscussionThrough a direct antemortem-to-postmortem validation, our study highlights the importance of understanding heterogeneity in AD in relation to concomitance of AD and non-AD pathologies. Our findings provide a deeper understanding of both global and regional vulnerabilities of the biological subtypes of AD brain towards (co)-pathologies. Relative involvement of both AD hallmark and non-AD (co)-pathologies will enhance prevailing knowledge of biological heterogeneity in AD and could thus, contribute towards tracking disease progression and designing clinical trials in the future.

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