P4-079 Is variation in the gene encoding insulin-degrading enzyme (IDE) a risk factor in late-onset Alzheimer's disease?

2004 ◽  
Vol 25 ◽  
pp. S496-S497
Author(s):  
Petra Nowotny ◽  
Scott Smemo ◽  
Tony Hinrichs ◽  
Peter Holmans ◽  
Kristina Tracey ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Factor ◽  
Late Onset ◽  
Insulin Degrading Enzyme ◽  
Gene Encoding ◽  
Degrading Enzyme

Substantial linkage disequilibrium across the insulin-degrading enzyme locus but no association with late-onset Alzheimer's disease

2001 ◽  
Vol 109 (6) ◽  
pp. 646-652 ◽  
Author(s):  
Richard Abraham ◽  
Amanda Myers ◽  
Fabienne Wavrant-DeVrieze ◽  
Marian L. Hamshere ◽  
Hollie V. Thomas ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Linkage Disequilibrium ◽  
Late Onset ◽  
Enzyme Locus ◽  
Insulin Degrading Enzyme ◽  
Degrading Enzyme

scholarly journals Reduced Hippocampal Insulin-Degrading Enzyme in Late-Onset Alzheimer's Disease Is Associated with the Apolipoprotein E-ε4 Allele

2003 ◽  
Vol 162 (1) ◽  
pp. 313-319 ◽  
Author(s):  
David G. Cook ◽  
James B. Leverenz ◽  
Pamela J. McMillan ◽  
J. Jacob Kulstad ◽  
Sasha Ericksen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Apolipoprotein E ◽  
Late Onset ◽  
Insulin Degrading Enzyme ◽  
Degrading Enzyme ◽  
Ε4 Allele

P3-244: Insulin degrading enzyme and the risk of late-onset Alzheimer's disease: A large replication study in a European population

2008 ◽  
Vol 4 ◽  
pp. T592-T592
Author(s):  
Kevin Morgan ◽  
Minerva Carrasquillo ◽  
Olivia Belbin ◽  
Kristelle Brown ◽  
Noor Kalsheker ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Late Onset ◽  
European Population ◽  
Replication Study ◽  
Insulin Degrading Enzyme ◽  
Degrading Enzyme

P1-312: Successful replication of association between late-onset Alzheimer's disease and the Insulin degrading enzyme (IDE)

2006 ◽  
Vol 2 ◽  
pp. S188-S188
Author(s):  
Behnosh Fakhri Björk ◽  
Hagit Katzov ◽  
Patrick Kehoe ◽  
Laura Fratiglioni ◽  
Bengt Winblad ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Late Onset ◽  
Insulin Degrading Enzyme ◽  
Degrading Enzyme ◽  
Successful Replication

P1-310: Late onset Alzheimer's disease (LOAD) susceptibility alleles in the insulin-degrading-enzyme gene (IDE ) and other Aβ-degrading enzymes

2006 ◽  
Vol 2 ◽  
pp. S187-S187
Author(s):  
Minerva M. Carrasquillo ◽  
Samuel G. Younkin ◽  
Mariah R. Kashino ◽  
Samantha L. Wilcox ◽  
Toros A. Dincman ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Late Onset ◽  
Insulin Degrading Enzyme ◽  
Enzyme Gene ◽  
Degrading Enzyme ◽  
Degrading Enzymes

Association studies between risk for late-onset Alzheimer's disease and variants in insulin degrading enzyme

2005 ◽  
Vol 136B (1) ◽  
pp. 62-68 ◽  
Author(s):  
Petra Nowotny ◽  
Anthony L. Hinrichs ◽  
Scott Smemo ◽  
John S.K. Kauwe ◽  
Taylor Maxwell ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Late Onset ◽  
Association Studies ◽  
Insulin Degrading Enzyme ◽  
Degrading Enzyme

Characteristics of Insulin-degrading Enzyme in Alzheimer's Disease: A Meta-Analysis

2018 ◽  
Vol 15 (7) ◽  
pp. 610-617 ◽  
Author(s):  
Huifeng Zhang ◽  
Dan Liu ◽  
Huanhuan Huang ◽  
Yujia Zhao ◽  
Hui Zhou
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Enzyme Activity ◽  
Protein Level ◽  
Senile Plaque ◽  
Meta Analysis ◽  
Cochrane Library ◽  
Insulin Degrading Enzyme ◽  
Degrading Enzyme ◽  
Significant Difference

Background: β-amyloid (Aβ) accumulates abnormally to senile plaque which is the initiator of Alzheimer's disease (AD). As one of the Aβ-degrading enzymes, Insulin-degrading enzyme (IDE) remains controversial for its protein level and activity in Alzheimer's brain. Methods: The electronic databases PubMed, EMBASE, The Cochrane Library, OVID and Sinomed were systemically searched up to Sep. 20th, 2017. And the published case-control or cohort studies were retrieved to perform the meta-analysis. Results: Seven studies for IDE protein level (AD cases = 293; controls = 126), three for mRNA level (AD cases = 138; controls = 81), and three for enzyme activity (AD cases = 123; controls = 75) were pooling together. The IDE protein level was significantly lower in AD cases than in controls (SMD = - 0.47, 95% CI [-0.69, -0.24], p < 0.001), but IDE mRNA and enzyme activity had no significant difference (SMD = 0.02, 95% CI [-0.40, 0.43] and SMD = 0.06, 95% CI [-0.41, 0.53] respectively). Subgroup analyses found that IDE protein level was decreased in both cortex and hippocampus of AD cases (SMD = -0.43, 95% CI [-0.71, -0.16], p = 0.002 and SMD = -0.53, 95% CI [-0.91, -0.15], p = 0.006 respectively). However, IDE mRNA was higher in cortex of AD cases (SMD = 0.71, 95% CI [0.14, 1.29], p = 0.01), not in hippocampus (SMD = -0.26, 95% CI [-0.58, 0.06]). Conclusions: Our results indicate that AD patients may have lower IDE protease level. Further relevant studies are still needed to verify whether IDE is one of the factors affecting Aβ abnormal accumulation and throw new insights for AD detection or therapy.

scholarly journals Emerging evidence for associations between periodontitis and the development of Alzheimer’s disease

2014 ◽  
Vol 5 (1) ◽  
pp. 38-42 ◽  
Author(s):  
Sophie Poole ◽  
Sim K Singhrao ◽  
St John Crean
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Factor ◽  
Immune Responses ◽  
Periodontal Disease ◽  
Potential Risk ◽  
Inflammatory Disease ◽  
Pathogenic Bacteria ◽  
Late Onset ◽  
Systemic Circulation

Periodontal disease (PD) is an inflammatory disease affecting tooth-supporting tissues in which interaction of specific bacteria and the host’s immune responses play a pivotal role. The pathogenic bacteria associated with PD are a source of systemic inflammation as they have the ability to enter systemic circulation during everyday tasks such as brushing teeth and chewing food. Alzheimer’s disease (AD) is a form of dementia whereby inflammation is thought to play a key role in its pathogenesis and the risk of developing the disease increasing with age. The exact aetiology of the late-onset AD is unknown but peripheral infections are being considered as a potential risk factor.

scholarly journals ApoE4 attenuates cortical neuronal activity and impairs memory in young apoE4 rats

2021 ◽  
Author(s):  
Ilona Har-Paz ◽  
Elor Arieli ◽  
Anan Moran
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Factor ◽  
Neuronal Activity ◽  
Genetic Risk ◽  
Cortical Neurons ◽  
Late Onset ◽  
Genetic Risk Factor ◽  
Normal Brain ◽  
Brain Functions

AbstractThe E4 allele of apolipoprotein E (apoE4) is the strongest genetic risk factor for late-onset Alzheimer’s disease (AD). However, apoE4 may cause innate brain abnormalities before the appearance of AD related neuropathology. Understanding these primary dysfunctions is vital for early detection of AD and the development of therapeutic strategies for it. Recently we have shown impaired extra-hippocampal memory in young apoE4 mice – a deficit that was correlated with attenuated structural pre-synaptic plasticity in cortical and subcortical regions. Here we test the hypothesis that these early structural deficits impact learning via changes in basal and stimuli evoked neuronal activity. We recorded extracellular neuronal activity from the gustatory cortex (GC) of three-month-old humanized apoE4 and wildtype rats, before and after conditioned taste aversion (CTA) training. Despite normal sucrose drinking behavior before CTA, young apoE4 rats showed impaired CTA learning, consistent with our previous results in apoE4 mice. This behavioral deficit was correlated with decreased basal and taste-evoked firing rates in both putative excitatory and inhibitory GC neurons. Single neuron and ensemble analyses of taste coding demonstrated that apoE4 neurons could be used to correctly classify tastes, but were unable to undergo plasticity to support learning. Our results suggest that apoE4 impacts brain excitability and plasticity early in life and may act as an initiator for later AD pathologies.Significant statementThe ApoE4 allele is the strongest genetic risk-factor for late-onset Alzheimer’s disease (AD), yet the link between apoE4 and AD is still unclear. Recent molecular and in-vitro studies suggest that apoE4 interferes with normal brain functions decades before the development of its related AD neuropathology. Here we recorded the activity of cortical neurons from young apoE4 rats during extra-hippocampal learning to study early apoE4 neuronal activity abnormalities, and their effects over coding capacities. We show that apoE4 drastically reduces basal and stimuli-evoked cortical activity in both excitatory and inhibitory neurons. The apoE4-induced activity attenuation did not prevent coding of stimuli identity and valence, but impaired capacity to undergo activity changes to support learning. Our findings support the hypothesis that apoE4 interfere with normal neuronal plasticity early in life; a deficit that may lead to late-onset AD development.

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