scholarly journals Prior Intra-operative Hypotension is not a Risk Factor for Development of Alzheimer’s Disease

Author(s):  
N.I. Bohnen ◽  
E.F.M. Wijdicks ◽  
E. Kokmen ◽  
M.A. Warner ◽  
L.T. Kurland

ABSTRACT:Objective:A retrospective, population-based, case-control study was carried out to evaluate episodes of prior intra-operative hypotension as a potential risk factor for Alzheimer’s disease (AD).Methods:Patients were all incident cases of AD from 1975–1984 who resided for 40 years or more in Olmsted County prior to their onset of dementia (N = 252). One age and gender-matched control for each case was selected from all registrations for care at Mayo Clinic during the year of onset in the incident case. Each case and control group had 252 individuals.Results:Of these, 27 cases and 32 controls had at least one ten minute or longer episode of intra-operative hypotension of a systolic blood pressure of less than 90 mm Hg prior to the year of onset of dementia in the matched AD patient. We did not find a significantly increased risk of AD for hypotensive episodes of less than 75 or 90 mm Hg.Conclusions:It is unlikely that intra-operative hypotensive events of this degree increase the risk of AD.

2002 ◽  
Vol 14 (3) ◽  
pp. 239-248 ◽  
Author(s):  
Linda B. Hassing ◽  
Boo Johansson ◽  
Sven E. Nilsson ◽  
Stig Berg ◽  
Nancy L. Pedersen ◽  
...  

Background: The purpose of this study was to examine if Type 2 diabetes mellitus is a risk factor for dementia in very old age, specifically for Alzheimer's disease (AD) and vascular dementia (VaD). Methods: We evaluated the risk of dementia in relation to Type 2 diabetes using a population-based sample of 702 individuals aged 80 years and older (mean age 83 years). A total of 187 persons received a dementia diagnosis. Thirty-one individuals had a diabetes diagnosis prior to onset of the dementia. Results: Cox proportional hazard analyses, adjusted for age, gender, education, smoking habits, and circulatory diseases, indicated an elevated risk to develop VaD (relative risk = 2.54, 95% confidence interval 1.35–4.78) in individuals with diabetes mellitus. No association was found between diabetes and AD. Conclusion: Type 2 diabetes is selectively related to the different subtypes of dementia. There is no increased risk of AD but more than a twofold risk of VaD in persons with diabetes.


2020 ◽  
Vol 4 (1) ◽  
pp. 399-404
Author(s):  
Sara Ben Zaken ◽  
Zorian Radomysky ◽  
Gideon Koren

Background: High magnesium intake has been associated with a decreased risk of dementia. In contrast, other research has found that both low and high serum magnesium levels were associated with an increased risk of Alzheimer’s disease and mixed dementia. Hence, presently the role of magnesium levels in dementia is unclear. Objective: To investigate a possible association between serum magnesium concentrations and dementia in a large population-based sample. Methods: Maccabi Healthcare Service in Israel provides healthcare to over 2 million citizens. Maccabi maintains a registry with approximately 26,000 diagnosed dementia patients. We focused on patients of both sexes with Alzheimer’s disease or mixed dementia aged 65 or older, excluding patients with clinical diagnoses that could affect serum magnesium level, or with other causes of cognitive decline. Our control group consisted of patients of the same age and sex without dementia. Results: No significant differences were found in mean, mode, and median magnesium levels between the dementia and control groups. However, there were marginally but significantly more cases with low magnesium levels among dementia patients than among controls: A total of 9.4% of tests done in patients with dementia and 7.81% done in non-dementia subjects were hypomagnesemic (p <  0.00001). Conclusion: Despite similar means and medians of serum magnesium in dementia and controls, the proportion of lower than normal magnesium test results was slightly higher among dementia patients. It is possible that patients with dementia have more episodes of hypomagnesemia than controls, despite similar overall mean levels of magnesium.


Medicina ◽  
2019 ◽  
Vol 55 (10) ◽  
pp. 689
Author(s):  
Pšemeneckienė ◽  
Petrikonis ◽  
Rastenytė

Background and objective: Neuroinflammation is one of the pathological pathways of Alzheimer’s disease (AD), mediating the progression of neurodegeneration. Polymorphisms of proinflammatory cytokines have been linked to increased AD risk. Identification of certain combinations of polymorphisms could help predict disease in its preclinical stage. The aim of the study was to evaluate differences in the prevalence of TNFα –850T (rs1799724), IL1A –889T (rs1800587), and IL6 –174C (rs1800795, Intron type) polymorphisms between AD patients and healthy controls (HC) and determine the impact of these SNPs in combination with the APOEε4 allele on AD risk. Materials and Methods: The study population is comprised of 107 patients with sporadic AD (AD group) and age- and gender-matched 110 persons without impaired cognitive functions (control group). TNFα –850C > T polymorphism was revealed by a PCR and restriction fragment length polymorphism (RFLP) method. Real time PCR was used for IL1A and IL6 SNP genotyping. APOEε genotyping was done via hybridization method. Results: The frequencies of TNFα –850T, IL1A –889T, IL6 –174C allele and genotype did not differ between the AD and HC groups (p > 0.05). IL6 –174C was not in HWE, and it was not analysed further. APOEε4 allele (p = 0.001) and 3/4 and 4/4 genotypes (p = 0.005) were more prevalent in AD patients. APOEε4 carriage increased the risk of AD (OR 2.65, p = 0.001), while TNFα –850T and IL1A –889T polymorphisms were not found as significant independent risk factors for AD. The presence of at least one IL1A –889T allele in combination with APOEε4+ was associated with a lower risk of AD (OR 2.24, p = 0.047) than the carriage of APOEε4+ alone (OR 2.70, p = 0.015). Conclusions: No significant differences of TNFα –850, IL1A –889, and IL6 –174 polymorphisms frequencies were found between AD and control groups. In APOEε4 carriers IL1A –889T polymorphism was found to reduce the AD risk determined by APOEε4 alone.


BMJ Open ◽  
2014 ◽  
Vol 4 (10) ◽  
pp. e005627 ◽  
Author(s):  
Paolo Demurtas ◽  
Germano Orrù ◽  
Pierpaolo Coni ◽  
Luigi Minerba ◽  
Michela Corrias ◽  
...  

ObjectiveThe purpose of the study was to examine whether the insertion (I) and/or deletion (D) polymorphism of ACE confers susceptibility to primary pterygium in Sardinian patients in a case–control study.Methods and resultsPolymorphism genotyping was performed by nested PCR using genomic DNA extracted from the whole peripheral blood of participants with (n=251) and without (n=260) pterygium. DD, ID and II genotype frequencies were: 48%, 39% and 13%, respectively, for patients with pterygium, and 15%, 40% and 44%, respectively, for the control group. A statistically significant difference was found between the pterygium and control groups for the ACE I/D polymorphism (p<0.001). Moreover, a statistically significant difference was found between the DD and II groups (p<0.01; OR=10.49; 95% CI 6.18 to 17.79), DD+ID versus II group (p<0.01; OR=5.23; 95% CI 3.37 to 8.13) and DD versus ID groups (p<0.01; OR=3.21; 95% CI 2.04 to 5.04).ConclusionsStatistical analysis showed that the DD genotype is associated with an increased risk of developing pterygium, and with a good chance that the D allele may play an important role in the development of disease.


2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Hao-Lun Sun ◽  
Wei-Wei Li ◽  
Chi Zhu ◽  
Wang-Sheng Jin ◽  
Yu-Hui Liu ◽  
...  

Purpose. Recent study shows that blood-derived amyloid-beta (Aβ) can induce cerebral amyloidosis and is involved in the pathogenesis of Alzheimer’s disease (AD). The vast majority of blood Aβ is generated from platelet. Whether blood Aβ levels are associated with the count of platelets remains unknown. Methods. 58 clinically diagnosed AD patients, 18 11C-PIB-PET diagnosed AD patients, and 61 age- and gender-matched cognitively normal controls were included to analyze the correlation of plasma Aβ levels with platelet count. 13 AD patients and 40 controls with cerebrospinal fluid (CSF) samples were included to further analyze the correlation of CSF Aβ levels with platelet count. Aβ40 and Aβ42 levels in plasma and CSF were measured by ELISA kits. Results. The plasma Aβ42 level was positively correlated with platelet count in both AD patients and control group, especially in AD patients with positive PIB-PET, while there was no correlation as to Aβ40. The CSF Aβ levels also had no significant correlation with platelet count. Conclusion. It suggests that platelets may be involved in the pathogenesis of AD and become a potential peripheral biomarker for AD.


Author(s):  
M.A.S. Pinhel ◽  
A.M. Crestani ◽  
G.F. Sousa-Amorim ◽  
M.L. Gregório ◽  
J.C. Cação ◽  
...  

Background: Genetic polymorphisms in genes regulating cholesterol metabolism have been suggested to risk factor of developing Alzheimer’s disease (AD). Objective: to analyze the frequency of polymorphisms apolipoprotein E (APOE-HhaI) and adenosine triphosphate binding cassette transporter 1 (ABCA1-StyI) in patients with late-onset AD. Design: case-control study. Participants: We studied 166 subjects (≥65 years old): Study Group (SG)- 88 patients and Control Group (CG)- 88 without dementia. Setting: The polymorphisms were determined using the polymorphism chain reaction and restriction fragment length polymorphism (PCR-RFLP) methods. It was applied Fisher's exact/chi-square tests (P<0.05). Results: Genotypes with APOE*4 prevailed in SG. The genotypic combination between APOE-HhaI and ABCA1-StyI polymorphisms showed a prevalence of heterozygous genotypes of risk for AD. Conclusion: Although genetic variants for ABCA1-StyI alone does not differentiate patients and controls, the G allele in synergy with APOE*4 allele is highlighted in patients suggesting the influence of ABCA1 in the disease.


2018 ◽  
Vol 29 (9) ◽  
pp. 3712-3724 ◽  
Author(s):  
Zahra Jafari ◽  
Jogender Mehla ◽  
Bryan E Kolb ◽  
Majid H Mohajerani

Abstract Besides well-known risk factors for Alzheimer’s disease (AD), stress, and in particular noise stress (NS), is a lifestyle risk factor common today. It is known that females are at a significantly greater risk of developing AD than males, and given that stress is a common adversity in females during pregnancy, we hypothesized that gestational noise exposure could exacerbate the postpartum development of the AD-like neuropathological changes during the life span. Pregnant APPNL-G-F/NL-G-F mice were randomly assigned to either the stress condition or control group. The stress group was exposed to the NS on gestational days 12–16, which resulted in a markedly higher hypothalamic–pituitary–adrenal (HPA) axis responsivity during the postpartum stage. Higher amyloid-β (Aβ) deposition and larger Aβ plaque size in the olfactory area were the early onset impacts of the gestational stress (GS) seen at the age of 4 months. This pattern of increased Aβ aggregation and larger plaque size were observed in various brain areas involved in both AD and stress regulation, especially in limbic structures, at the age of 6 months. The GS also produced anxiety-like behavior, deficits in learning and memory, and impaired motor coordination. The findings suggest that environmental stresses during pregnancy pose a potential risk factor in accelerating postpartum cognitive decline and AD-like neuropathological changes in the dams (mothers) later in life.


Author(s):  
Luigi Attademo ◽  
Francesco Bernardini

As a global problem that has increasingly been causing worldwide concern, air pollution poses a significant and serious environmental risk to health. Risks of cardiovascular and respiratory diseases, as well as various types of cancer, have been consistently associated with the exposure to air pollutants. More recently, various studies have also shown that the central nervous system is also attacked by air pollution. Air pollution appears to be strongly associated with a higher risk of cognitive defects, neurodevelopmental (e.g., schizophrenia) and neurodegenerative (e.g., Alzheimer’s disease) disorders. Subjects with schizophrenia, as well as subjects with Alzheimer’s disease, experience a variety of neuropsychological deficits and cognitive impairments. This determines an adverse effect on social and professional functioning, and it contributes to the long-term disease burden. However, no final conclusions have been drawn on the matter of the direct relationship between schizophrenia and Alzheimer’s disease. In recent years, the topic of urbanicity and mental health has become increasingly important. Urban exposure to environmental toxins and pollution is currently described as a reliable risk factor for schizophrenia and other psychoses, and it has been demonstrated more and more how exposure to air pollutants is associated with increased risk of dementia. Pathways by which air pollution can target and damage the brain, leading to an increased risk for developing schizophrenia and Alzheimer’s disease, are multiple and complex. Results from epidemiological studies suggest potential associations, but are still insufficient to confirm causality. Further studies are needed in order to verify this hypothesis. And if confirmed, the clinical implications could be of substantial relevance for both public and mental health.


Author(s):  
Macrina Tortajada-Soler ◽  
Leticia Sánchez-Valdeón ◽  
Marta Blanco-Nistal ◽  
José Alberto Benítez-Andrades ◽  
Cristina Liébana-Presa ◽  
...  

Background: Alzheimer’s disease (AD) which is the most common type of dementia is characterized by mental or cognitive disorders. People suffering with this condition find it inherently difficult to communicate and describe symptoms. As a consequence, both detection and treatment of comorbidities associated with Alzheimer’s disease are substantially impaired. Equally, action protocols in the case of emergencies must be clearly formulated and stated. Methods: We performed a bibliography search followed by an observational and cross-sectional study involving a thorough review of medical records. A group of AD patients was compared with a control group. Each group consisted of 100 people and were all León residents aged ≥65 years. Results: The following comorbidities were found to be associated with AD: cataracts, urinary incontinence, osteoarthritis, hearing loss, osteoporosis, and personality disorders. The most frequent comorbidities in the control group were the following: eye strain, stroke, vertigo, as well as circulatory and respiratory disorders. Comorbidities with a similar incidence in both groups included type 2 diabetes mellitus, glaucoma, depression, obesity, arthritis, and anxiety. We also reviewed emergency procedures employed in the case of an emergency involving an AD patient. Conclusions: Some comorbidities were present in both the AD and control groups, while others were found in the AD group and not in the control group, and vice versa.


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