scholarly journals The mismatch negativity as an index of cognitive decline for the early detection of Alzheimer’s disease

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Manuela Ruzzoli ◽  
Cornelia Pirulli ◽  
Veronica Mazza ◽  
Carlo Miniussi ◽  
Debora Brignani
2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Dalia Farouk Hussen ◽  
Ayat Allah Farouk Hussein ◽  
Mahmoud Abdel Moety Monzer ◽  
Saida Ali Hammad

Abstract Background Alzheimer’s disease (AD) is the most widely recognized type of dementia. It is associated with cell cycle abnormalities including genomic instability and increased micronuclei (MNi) which usually evolve many years before the appearance of the clinical manifestations. Digital electroencephalogram (EEG) has a role in perceiving brain changes in dementia and in early detection of cognitive decline. This study aimed to assess the competency of using neurophysiological markers including absolute power of alpha waves and a cytogenetic marker which comprises scoring of MNi as a step toward early and preclinical diagnosis of AD. The study was conducted on 27 subjects; they were 15 patients diagnosed as sporadic AD and a group of 12 age and sex-matched controls. All subjects were subjected to Mini-Mental State Examination (MMSE), conventional EEG, digital EEG, and cytokinesis-block micronucleus assay (CBMN) in peripheral blood lymphocytes. Results Conventional EEG showed a normal background activity with no abnormal epileptogenic discharges in both groups. Digital EEG showed significant reduction of the absolute power of alpha waves for AD patients as compared to the control group (P < 0.0001). Score of MNi showed statistical significant difference between the two groups (P < 0.0001). By linking scores of both cognitive state using MMSE and MNi among the group of patients, a significant negative correlation was detected (r = −0.6066). The correlations between cognitive state and the absolute power of alpha wave among the patients revealed a positive correlation (r = 0.2235). Conclusions The combination of both cytogenetic and neurophysiological markers can be beneficial for early detection of cognitive decline and may lead to preclinical identification of individuals at increased risk for AD, where at this stage treatment is constructive. The negative correlation between the scores of MNi and MMSE is suggestive for the impact of genomic instability on the cognitive state.


2018 ◽  
Vol 15 (3) ◽  
pp. 219-228 ◽  
Author(s):  
Jiri Cerman ◽  
Ross Andel ◽  
Jan Laczo ◽  
Martin Vyhnalek ◽  
Zuzana Nedelska ◽  
...  

Background: Great effort has been put into developing simple and feasible tools capable to detect Alzheimer's disease (AD) in its early clinical stage. Spatial navigation impairment occurs very early in AD and is detectable even in the stage of mild cognitive impairment (MCI). Objective: The aim was to describe the frequency of self-reported spatial navigation complaints in patients with subjective cognitive decline (SCD), amnestic and non-amnestic MCI (aMCI, naMCI) and AD dementia and to assess whether a simple questionnaire based on these complaints may be used to detect early AD. Method: In total 184 subjects: patients with aMCI (n=61), naMCI (n=27), SCD (n=63), dementia due to AD (n=20) and normal controls (n=13) were recruited. The subjects underwent neuropsychological examination and were administered a questionnaire addressing spatial navigation complaints. Responses to the 15 items questionnaire were scaled into four categories (no, minor, moderate and major complaints). Results: 55% of patients with aMCI, 64% with naMCI, 68% with SCD and 72% with AD complained about their spatial navigation. 38-61% of these complaints were moderate or major. Only 33% normal controls expressed complaints and none was ranked as moderate or major. The SCD, aMCI and AD dementia patients were more likely to express complaints than normal controls (p's<0.050) after adjusting for age, education, sex, depressive symptoms (OR for SCD=4.00, aMCI=3.90, AD dementia=7.02) or anxiety (OR for SCD=3.59, aMCI=3.64, AD dementia=6.41). Conclusion: Spatial navigation complaints are a frequent symptom not only in AD, but also in SCD and aMCI and can potentially be detected by a simple and inexpensive questionnaire.


2018 ◽  
Vol 15 (4) ◽  
pp. 386-398 ◽  
Author(s):  
Fabricio Ferreira de Oliveira ◽  
Elizabeth Suchi Chen ◽  
Marilia Cardoso Smith ◽  
Paulo Henrique Ferreira Bertolucci

Background: While the angiotensin-converting enzyme degrades amyloid-β, angiotensinconverting enzyme inhibitors (ACEis) may slow cognitive decline by way of cholinergic effects, by increasing brain substance P and boosting the activity of neprilysin, and by modulating glucose homeostasis and augmenting the secretion of adipokines to enhance insulin sensitivity in patients with Alzheimer’s disease dementia (AD). We aimed to investigate whether ACE gene polymorphisms rs1800764 and rs4291 are associated with cognitive and functional change in patients with AD, while also taking APOE haplotypes and anti-hypertensive treatment with ACEis into account for stratification. Methods: Consecutive late-onset AD patients were screened with cognitive tests, while their caregivers were queried for functional and caregiver burden scores. Prospective pharmacogenetic correlations were estimated for one year, considering APOE and ACE genotypes and haplotypes, and treatment with ACEis. Results: For 193 patients, minor allele frequencies were 0.497 for rs1800764 – C (44.6% heterozygotes) and 0.345 for rs4291 – T (38.9% heterozygotes), both in Hardy-Weinberg equilibrium. Almost 94% of all patients used cholinesterase inhibitors, while 155 (80.3%) had arterial hypertension, and 124 used ACEis. No functional impacts were found regarding any genotypes or pharmacological treatment. Either for carriers of ACE haplotypes that included rs1800764 – T and rs4291 – A, or for APOE4- carriers of rs1800764 – T or rs4291 – T, ACEis slowed cognitive decline independently of blood pressure variations. APOE4+ carriers were not responsive to treatment with ACEis. Conclusion: ACEis may slow cognitive decline for patients with AD, more remarkably for APOE4- carriers of specific ACE genotypes.


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