scholarly journals Genetic Association between Presenilin 2 Polymorphisms and Alzheimer's Disease and Dementia of Lewy Body Type in a Japanese Population

2016 ◽  
Vol 6 (1) ◽  
pp. 90-97 ◽  
Author(s):  
Ayako Suzuki ◽  
Nobuto Shibata ◽  
Koji Kasanuki ◽  
Tomoyuki Nagata ◽  
Shunichiro Shinagawa ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Lewy Body ◽  
Japanese Population ◽  
Psychological Symptoms ◽  
Lewy Body Dementia ◽  
Nucleotide Polymorphisms ◽  
Genetic Associations ◽  
Body Type ◽  
Presenilin 2

Background/Aims: Mutations in the presenilin 2 (PSEN2) gene cause familial Alzheimer's disease (AD). Common polymorphisms affect gene activity and increase the risk of AD. Nonsynonymous polymorphisms in the PSEN2 gene showed Lewy body dementia (LBD) phenotypes clinically. Therefore, we aimed to investigate whether PSEN2 gene polymorphisms were associated with AD or LBD. Methods: Seven single nucleotide polymorphisms (SNPs) of the gene were analyzed using a case-control study design comprising 288 AD patients, 76 LBD patients, and 105 age-matched controls. Results: Linkage disequilibrium (LD) examination showed strong LD from rs1295645 to rs8383 on the gene in our cases from Japan. There were no associations between the SNPs studied here and AD onset, and haplotypic analyses did not detect genetic associations between AD and the PSEN2 gene. Although the number of the cases was small, the SNPs studied did not modify the risk of developing LBD in a Japanese population. Conclusion: The common SNPs of the PSEN2 gene did not affect the risk of AD or LBD in a Japanese population. Because genetic variability of the PSEN2 gene is associated with behavioral and psychological symptoms of dementia (BPSD) in AD and LBD, further detailed analyses considering BPSD of both diseases would be required.

Dementia with Lewy bodies

1998 ◽  
Vol 4 (6) ◽  
pp. 360-363 ◽  
Author(s):  
E. Jane Byrne
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Lewy Body ◽  
Senile Dementia ◽  
Lewy Bodies ◽  
Lewy Body Dementia ◽  
Body Type ◽  
Clinical Criteria ◽  
Dementia Syndrome ◽  
Distinct Disease

Dementia with cortical Lewy bodies (LBD) was first described by Okazakiet alin 1961 and is now recognised as a relatively common cause of the dementia syndrome. The true prevalence of LBD is unknown. In post-mortem studies of patients diagnosed as having dementia in life, the mean frequency of Lewy body dementia is 12.5% (Byrne, 1997). Clinically diagnosed LBD (using operational clinical criteria) is found in 10–23% of patients presenting to, or in the care of, psychogeriatric services (Collertonet al, 1996). What is not yet certain is its nosological status; opinion is divided between regarding it as a variety of Alzheimer's disease (the Lewy body variant), a distinct disease (senile dementia of the Lewy body type) or a spectrum disorder related to both Parkinson's disease and to Alzheimer's disease (Byrne, 1992).

scholarly journals Functional connectivity of the nucleus basalis of Meynert in Lewy body dementia and Alzheimer’s disease

2021 ◽  
pp. 1-6
Author(s):  
Julia Schumacher ◽  
Alan J. Thomas ◽  
Luis R. Peraza ◽  
Michael Firbank ◽  
John T. O’Brien ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Functional Connectivity ◽  
Lewy Body ◽  
Cholinergic System ◽  
Structural Changes ◽  
Lewy Body Dementia ◽  
Occipital Cortex ◽  
Nucleus Basalis ◽  
Nucleus Basalis Of Meynert

ABSTRACT Cholinergic deficits are a hallmark of Alzheimer’s disease (AD) and Lewy body dementia (LBD). The nucleus basalis of Meynert (NBM) provides the major source of cortical cholinergic input; studying its functional connectivity might, therefore, provide a tool for probing the cholinergic system and its degeneration in neurodegenerative diseases. Forty-six LBD patients, 29 AD patients, and 31 healthy age-matched controls underwent resting-state functional magnetic resonance imaging (fMRI). A seed-based analysis was applied with seeds in the left and right NBM to assess functional connectivity between the NBM and the rest of the brain. We found a shift from anticorrelation in controls to positive correlations in LBD between the right/left NBM and clusters in right/left occipital cortex. Our results indicate that there is an imbalance in functional connectivity between the NBM and primary visual areas in LBD, which provides new insights into alterations within a part of the corticopetal cholinergic system that go beyond structural changes.

scholarly journals Benzodiazepines and antidepressants: effects on cognitive and functional decline in Alzheimer’s disease and Lewy body dementia

2020 ◽  
Author(s):  
Miguel Germán Borda ◽  
Alberto Jaramillo‐Jimenez ◽  
Ragnhild Oesterhus ◽  
Jose Manuel Santacruz ◽  
Diego Alejandro Tovar‐Rios ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Lewy Body ◽  
Functional Decline ◽  
Lewy Body Dementia

P3-259: Mechanisms of psychomotor slowing in Alzheimer's disease and Lewy body dementia

2012 ◽  
Vol 8 (4S_Part_15) ◽  
pp. P550-P550
Author(s):  
Martine Roussel ◽  
Olivier Bailon ◽  
Olivier Godefroy
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Lewy Body ◽  
Lewy Body Dementia ◽  
Psychomotor Slowing

scholarly journals Cerebrospinal Fluid Levels of sAPPαand sAPPβin Lewy Body and Alzheimer's Disease: Clinical and Neurochemical Correlates

2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
Ezra Mulugeta ◽  
Elisabet Londos ◽  
Oskar Hansson ◽  
Clive Ballard ◽  
Ragnhild Skogseth ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebrospinal Fluid ◽  
Lewy Body ◽  
Group Analysis ◽  
Lewy Body Dementia ◽  
Csf Biomarkers ◽  
Commercial Kits ◽  
Neurochemical Correlates ◽  
Fluid Levels

We measured cerebrospinal fluid (CSF) levels of the soluble isoforms of amyloid precursor protein (APP; sAPPαsAPPβ) and other CSF biomarkers in 107 patients with Alzheimer's disease (AD), dementia with Lewy body dementia (DLB), Parkinson's disease dementia (PDD), and normal controls (NC) using commercial kits. DLB and PDD were combined in a Lewy body dementia group (LBD). No differences were observed in sAPPαand sAPPβlevels between the groups. Significant correlations were observed between sAPPαand sAPPβand between sAPPβand Mini-Mental State Examination scores in the total group analysis as well as when LBD and AD groups were analyzed separately. sAPPαand sAPPβlevels correlated with Aβ38, Aβ40, Aβ42, and Tau in the LBD group. In AD, sAPPαcorrelated with p-Tau and sAPPβwith Aβ40. The differential association between sAPPαand sAPPβwith Aβand Tau species between LBD and AD groups suggests a possible relationship with the underlying pathologies in LBD and AD.

scholarly journals Collusion of α-Synuclein and Aβ aggravating co-morbidities in a novel prion-type mouse model

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Grace M. Lloyd ◽  
Jess-Karan S. Dhillon ◽  
Kimberly-Marie M. Gorion ◽  
Cara Riffe ◽  
Susan E. Fromholt ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Lewy Body ◽  
Amyloid Β ◽  
Lewy Body Dementia ◽  
Immunohistochemical Analysis ◽  
Aggregation Kinetics ◽  
Current Area ◽  
Old Mice ◽  
A Current

Abstract Background The misfolding of host-encoded proteins into pathological prion conformations is a defining characteristic of many neurodegenerative disorders, including Alzheimer’s disease, Parkinson’s disease, and Lewy body dementia. A current area of intense study is the way in which the pathological deposition of these proteins might influence each other, as various combinations of co-pathology between prion-capable proteins are associated with exacerbation of disease. A spectrum of pathological, genetic and biochemical evidence provides credence to the notion that amyloid β (Aβ) accumulation can induce and promote α-synuclein pathology, driving neurodegeneration. Methods To assess the interplay between α-synuclein and Aβ on protein aggregation kinetics, we crossed mice expressing human α-synuclein (M20) with APPswe/PS1dE9 transgenic mice (L85) to generate M20/L85 mice. We then injected α-synuclein preformed fibrils (PFFs) unilaterally into the hippocampus of 6-month-old mice, harvesting 2 or 4 months later. Results Immunohistochemical analysis of M20/L85 mice revealed that pre-existing Aβ plaques exacerbate the spread and deposition of induced α-synuclein pathology. This process was associated with increased neuroinflammation. Unexpectedly, the injection of α-synuclein PFFs in L85 mice enhanced the deposition of Aβ; whereas the level of Aβ deposition in M20/L85 bigenic mice, injected with α-synuclein PFFs, did not differ from that of mice injected with PBS. Conclusions These studies reveal novel and unexpected interplays between α-synuclein pathology, Aβ and neuroinflammation in mice that recapitulate the pathology of Alzheimer’s disease and Lewy body dementia.

Risk of Hospitalization in Patients with Alzheimer’s Disease and Lewy Body Dementia: Time to and Length of Stay

2020 ◽  
Vol 74 (4) ◽  
pp. 1221-1230
Author(s):  
Ragnhild Oesterhus ◽  
Ingvild Dalen ◽  
Anne Katrine Bergland ◽  
Dag Aarsland ◽  
Svein R. Kjosavik
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Length Of Stay ◽  
Lewy Body ◽  
Lewy Body Dementia

scholarly journals Neuropsychiatric symptoms correlated with functional trajectories among people living with Alzheimer’s disease dementia and Lewy body dementia

2020 ◽  
Vol 16 (S8) ◽  
Author(s):  
Miguel German Borda ◽  
Dag Aarsland ◽  
Ketil Oppedal ◽  
Lasse Melvær Giil ◽  
Audun Osland Vik‐Mo ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Lewy Body ◽  
Neuropsychiatric Symptoms ◽  
Lewy Body Dementia ◽  
Alzheimer’S Disease Dementia
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