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 Alzheimer's disease cerebrospinal fluid biomarkers predict cognitive decline in lewy body dementia

2016 ◽  
Vol 31 (8) ◽  
pp. 1203-1208 ◽  
Author(s):  
Carla Abdelnour ◽  
Inger van Steenoven ◽  
Elisabet Londos ◽  
Frédéric Blanc ◽  
Bjørn Auestad ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebrospinal Fluid ◽  
Cognitive Decline ◽  
Lewy Body ◽  
Lewy Body Dementia ◽  
Cerebrospinal Fluid Biomarkers

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 Cerebrospinal Fluid Biomarkers of Alzheimer’s Disease: Current Evidence and Future Perspectives

2021 ◽  
Vol 11 (2) ◽  
pp. 215
Author(s):  
Donovan A. McGrowder ◽  
Fabian Miller ◽  
Kurt Vaz ◽  
Chukwuemeka Nwokocha ◽  
Cameil Wilson-Clarke ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebrospinal Fluid ◽  
Late Onset ◽  
Amyloid Β ◽  
Current Evidence ◽  
Csf Biomarkers ◽  
Diagnostic Efficacy ◽  
Neurofilament Light ◽  
New Biomarkers

Alzheimer’s disease is a progressive, clinically heterogeneous, and particularly complex neurodegenerative disease characterized by a decline in cognition. Over the last two decades, there has been significant growth in the investigation of cerebrospinal fluid (CSF) biomarkers for Alzheimer’s disease. This review presents current evidence from many clinical neurochemical studies, with findings that attest to the efficacy of existing core CSF biomarkers such as total tau, phosphorylated tau, and amyloid-β (Aβ42), which diagnose Alzheimer’s disease in the early and dementia stages of the disorder. The heterogeneity of the pathophysiology of the late-onset disease warrants the growth of the Alzheimer’s disease CSF biomarker toolbox; more biomarkers showing other aspects of the disease mechanism are needed. This review focuses on new biomarkers that track Alzheimer’s disease pathology, such as those that assess neuronal injury (VILIP-1 and neurofilament light), neuroinflammation (sTREM2, YKL-40, osteopontin, GFAP, progranulin, and MCP-1), synaptic dysfunction (SNAP-25 and GAP-43), vascular dysregulation (hFABP), as well as CSF α-synuclein levels and TDP-43 pathology. Some of these biomarkers are promising candidates as they are specific and predict future rates of cognitive decline. Findings from the combinations of subclasses of new Alzheimer’s disease biomarkers that improve their diagnostic efficacy in detecting associated pathological changes are also presented.

Cerebrospinal fluid levels of alpha-tocopherol (vitamin E) in Alzheimer's disease

1997 ◽  
Vol 104 (6-7) ◽  
pp. 703-710 ◽  
Author(s):  
F. J. Jiménez-Jiménez ◽  
F. de Bustos ◽  
J. A. Molina ◽  
J. Benito-León ◽  
A. Tallón-Barranco ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebrospinal Fluid ◽  
Vitamin E ◽  
Alpha Tocopherol ◽  
Cerebrospinal Fluid Levels ◽  
Fluid Levels

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 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.

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