Senior Moments Are Never-ending Times When You Are Old (Are They?): First Step of Turquoise Project.

Introduction: The number of dementia patients in Turkey is increasing, as well as all over the world. However, we do not know how much society knows about dementia. The aim of this study is to evaluate people's concept of dementia, their awareness of dementia research and treatment, whether dementia and forgetfulness are considered normal in old age, and whether having dementia is associated with a lack of mental abilities. Methods: A Dementia Awareness Questionnaire was created in the form of a self-report questionnaire, consisting of 20 questions and using a five-point Likert-type answering method in order to question participants' information about dementia. In addition, we asked for demographic information such as age, gender, occupation, education level of the participants, as well as whether they have had relatives diagnosed with a neurodegenerative disease. The surveys were administered online. Results: A total of 1551 participants from 53 cities were included in the study. Approximately half of the participants did not know the definition of dementia, 20.9% thought that dementia and Alzheimer's disease were the same; 50.4% considered forgetfulness, and 55.2% considered dementia as a natural consequence of aging. While 34.5% of the participants thought that dementia patients could be dangerous, 10.3% thought they could not continue living as a part of society. While 38.5% of healthcare professionals do not know the definition of dementia, 18.5% of them say that dementia and Alzheimer's disease are the same, 58.5% think that dementia patients are not fit to make their own decisions, 40.6% believe that dementia patients have criminal liability. 15.8% of healthcare professionals thought that dementia is only seen in elderly people; 21.4% thought that dementia, and 49.2% thought that forgetfulness was a result of normal aging. Conclusion: Our study confirms that dementia is still an unknown concept in society and among healthcare professionals. It is widely believed that forgetfulness and dementia are part of normal aging, and there is no cure for dementia. This study, which we have done in order to understand the level of dementia awareness in Turkish society, reveals the necessity for research on dementia and studies on how to increase dementia awareness.

DNA repair gene OGG1 polymorphism and its relation with oxidative DNA damage in patients with Alzheimer's disease.

There is considerable evidence that oxidative DNA damage is increased, DNA repair capacity is decreased in patients with Alzheimer's disease. Base excision repair is the major pathway in removal of oxidative DNA damage. 8-oxo-deoxyguanosine DNA glycosylase 1 (OGG1) is the enzyme which is involved in the first step of this repair process. Alterations in DNA repair capacity may be related with polymorphisms in DNA repair genes. In order to investigate the effect of OGG1 Ser326Cys polymorphism on oxidative DNA damage level, OGG1 genotyping was performed, basal and oxidative DNA damage in lymphocytes and 8-OHdG level in plasma were examined in patients with Alzheimer's disease. Basal and oxidative DNA damage and 8-OHdG level were measured by OGG1-modified comet assay and enzyme-linked immunoassay, respectively. OGG1 genotyping was performed by polymerase chain reaction- restriction fragment length polymorphism assay. Basal and oxidative DNA damage and plasma 8-OHdG levels were found to be higher in the Alzheimer's disease group than those in the control group (P < 0.001). In the Alzheimer's disease group, the levels of oxidative DNA damage was higher in the patients having OGG1 (Ser326Cys + Cys326Cys) genotype than those in the patients having OGG1 Ser326Ser genotype. It was concluded that oxidative DNA damage is increased in patients with Alzheimer's disease and OGG1 Ser326Cys polymorphism may be responsible for this increase.

DNA damage, DNA susceptibility to oxidation and glutathione redox status in patients with Alzheimer's disease treated with and without memantine.

The aim of the current study was to compare oxidative DNA damage, DNA susceptibility to oxidation, and ratio of GSH/GSSG in patients with Alzheimer's disease (AD) treated with acetylcholinesterase inhibitor (AChEI) and combined AChEI+memantine. The study included 67 patients with AD and 42 volunteers as control. DNA damage parameters (strand breaks, oxidized purines, H2O2-induced DNA damage) in lymphocyte DNA and GSH/GSSG ratio in erythrocytes were determined by the comet assay and spectrophotometric assay, respectively. DNA damage was found to be higher, GSH/GSSG ratio was found to be lower in the AD group than those in the control group. DNA strand breaks and H2O2-induced DNA damage were lower in the patients taking AChEI+memantine than those in the patients taking AChEI but no significant difference was determined between the groups for oxidized purines and GSH/GSSG ratio. In conclusion, increased systemic oxidative DNA damage and DNA susceptibility to oxidation may be resulted from diminished GSH/GSSG ratio in AD patients. Although DNA strand breaks and H2O2-induced DNA damage are lower in the AD patients treated with combined AChEI and memantine, this may not indicate protective effect of memantine against DNA oxidation due to similar levels of oxidized purines in the patients treated with AChEI and AChEI+memantine.

Inflammatory hypothesis as a link between Alzheimer's disease and diabetes mellitus.

AIMS: The aim of the present study was to evaluate whether there was an inflammation-mediated link between Alzheimer's disease (AD) and type 2 diabetes mellitus (DM) status. METHODS: An age-matched control group and patient groups designated as AD without treatment (AD); AD under cholinesterase inhibitors (AD-CEI); DM without treatment (DM); DM under oral antidiabetic agents (DM-OAD); AD under treatment, who had newly diagnosed DM (AD-CEI+DM); and DM under treatment, who had newly diagnosed probable AD (DM-OAD+AD) were studied. Serum inflammation status was evaluated by the determination of serum C-reactive protein (CRP), tumor necrosis factor-alpha, interleukin (IL)-1ß and IL-6 levels. CRP levels were determined by an immunonephelometric method. The others were assayed by enzyme-linked immunosorbent assay methods. RESULTS: IL-1ß levels were found to be significantly lower in the DM group than in the control group (P < 0.01). The AD group had significantly higher serum IL-1ß levels than the DM group (P < 0.01). IL-6 levels were significantly higher in the AD and DM groups than in controls (P < 0.01 and P < 0.01). Serum tumor necrosis factor-alpha and CRP levels in the AD (P < 0.05 and P < 0.001, respectively) and DM groups (P < 0.05 and P < 0.001, respectively) were significantly higher when compared with the controls. The presence of AD or DM or therapies of the diseases did not significantly change in serum tumor necrosis factor-alpha levels. The AD-CEI + DM and DM-OAD+AD groups had significantly higher CRP levels than the AD-CEI group (P < 0.05) and DM-OAD groups (P < 0.001), respectively. Serum CRP levels showed a positive correlation with Mini-Mental State Examination scores (r = 0.339, P < 0.01). CONCLUSION: Our findings support the presence of a low-grade systemic inflammation link between AD and DM. Geriatr Gerontol Int 2016; 16: 1161-1166.

Hypercholesterolemia as one of the risk factors of intracerebral hemorrhage.

Stroke is still a major cause of morbidity and mortality throughout the world, although better stratification and treatment modalities are being developed. As compared to ischemic stroke, intracerebral hemorrhage (ICH) possesses many unknown data and lacks guidelines for better prophylaxis. In this study, we aimed to investigate patients with ICH hospitalized in our neurology department within 5 years in terms of risk stratification. A total of 4,449 patients were hospitalized; 1,378 of patients (31%) were diagnosed as having cerebrovascular disease and of these 165 patients (3.7%) had ICH. The risk factors of patients with ICH were investigated and compared with age- and gender matched 75 healthy subjects. We observed that hypercholesterolemia (p = 0.002) was one of the most common risk factors in patients with ICH as compared to controls, together with hypertension (p = 0.010). On the other hand, hypolipidemia (LDL-cholesterol level < 50 mg/dl) was not present in any of the patients. As our purpose as neurologists is to reduce the occurrence and fatal outcome of cerebrovascular events, we aimed to emphasize the importance of risk factors to be well defined, for which every effort should be exhibited for both primary and secondary prevention.

Serum brain-derived neurotrophic factor, nerve growth factor and neurotrophin-3 levels in dementia.

The aim of this study is to measure serum levels of neurotropic factor (NF) in patients with dementia. Brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), and neurotrophin-3 (NT-3) were determined in Alzheimer's dementia patients without medication (AD; n: 22), Alzheimer's dementia patients receiving cholinesterase inhibitor (CEI) treatment (AD + CEI; n: 32) and vascular dementia patients receiving CEI treatment (VaD + CEI; n: 27) and the age-matched control group (n: 20). NGF levels were detected to be significantly higher in the control group than in AD group (P < 0.001). BDNF and NT-3 levels in AD group were not significantly different from control group's levels. NGF levels in AD + CEI group were significantly higher than in AD group (P < 0.05). There was also no significant difference in serum neurotrophic factor levels between AD + CEI and VaD + CEI group. A positive correlation between BDNF and Mini Mental State Examination (MMSE) scores (r: 0.422, P < 0.01) in AD group and a negative correlation between BDNF and MMSE scores in the AD + CEI group (r: -0.357, P < 0.005) were obtained. In conclusion, our results suggest that while serum NGF levels are associated with the presence of dementia, serum BDNF levels may be associated with the severity of Alzheimer's dementia. However, future studies are required to determine the importance of NFs.

Somatosensory eye blink reflex in peripheral facial palsy.

To investigate the association between somatosensory blink reflex (SBR) and peripheral facial palsy (PFP) severity and trigeminal blink reflex (BR) changes in cases with PFP and subsequent postparalytic facial syndrome development (PFS). One hundred and twenty subjects with peripheral facial palsy and post-facial syndrome and 44 age and gender matched healthy volunteers were enrolled to this study. Blink reflexes and somatosensory blink reflex were studied in all. The association between R1 and R2 responses of the BR and SBR positivity was investigated. SBR was elicited in 36.3% of normal subjects, in 18.3% of PFP and in 65.3% of PFS patients. In the paralytic side, the frequency of SBR positivity was significantly lower in PFP group compared to controls and SBR was most frequently observed in patients with PFS. Compared to PFP and control groups, SBR positivity on the non-paralytic side significantly revealed a higher rate in PFS patients. SBR positivity of patients in whom R1 or R2 were absent, was significantly lower than those subjects with prolonged or normal R1 or R2 responses. PFP and successive PFS are good models for the sensory motor gate mechanisms and/or excitability enhancement of brainstem neurons responsible for SBR.

Spinal myoclonus following a peripheral nerve injury: a case report.

Spinal myoclonus is a rare disorder characterized by myoclonic movements in muscles that originate from several segments of the spinal cord and usually associated with laminectomy, spinal cord injury, post-operative, lumbosacral radiculopathy, spinal extradural block, myelopathy due to demyelination, cervical spondylosis and many other diseases. On rare occasions, it can originate from the peripheral nerve lesions and be mistaken for peripheral myoclonus. Careful history taking and electrophysiological evaluation is important in differential diagnosis. The aim of this report is to evaluate the clinical and electrophysiological characteristics and treatment results of a case with spinal myoclonus following a peripheral nerve injury without any structural lesion.

Fabry disease mimicking multiple sclerosis.

Fabry disease is an X-linked recessive lysosomal storage disorder resulting from the deficiency of alpha-galactosidase. This disease causes endothelial vasculopathy and affects multiple organ systems. Hemizygous male patients represent the classical renal, cardiac and neurological symptoms of disease. Heterozygous female carriers are frequently asymptomatic, but cerebrovascular events in females are as frequent as in males. Even if rarely seen, neurological damage is an important cause of morbidity. Severe neurological signs that are due to multifocal small vessel occlusions may be present without major thrombosis. In this report, we present a 33-year-old female patient with recurrent neurological deficits secondary to multifocal small vessel involvements. The case had previously been misdiagnosed as multiple sclerosis. Cerebral MRI revealed hyperintense lesions located in bilateral thalamus, supratentorial areas, and left cerebellum. Laboratory and radiological investigations were performed for differential diagnosis, but the etiology could not be identified. During follow-up period, skin lesions and proteinuria were detected. The dermatological, neurological, laboratory, and radiological findings were all suggestive of Fabry disease and the diagnosis was confirmed by subsequent enzyme assays. Fabry disease should be considered in young patients with unexplained stroke-like episodes, especially in those who have infarction in the vertebrobasilar arterial system, angiokeratomas, and proteinuria.

An association between mesial temporal lobe epilepsy with hippocampal sclerosis and human leukocyte antigens.

PURPOSE: Mesial temporal lobe epilepsy with hippocampal sclerosis (MTLE-HS) is one of the medically intractable epilepsies that may be remediable with surgery. Although the pathogenesis of HS still remains obscure, genetics may play a role as a predisposing factor, with the genetically controlled immune system as one of its aspects. Our aim in this study was to investigate whether there is any association between human leukocyte antigens (HLAs) that are related to chromosome 6 and this specific type of epilepsy. METHODS: HLA class I and II typing were performed with the microlymphocytotoxicity method on 65 Turkish patients with MTLE-HS and on 184 healthy controls. RESULTS: Our study revealed a significantly high frequency of class II antigens HLA-DQ2, -DR4, and -DR7 alleles and the combination of HLA-DR4-DQ2, and DR7-DQ2 alleles. CONCLUSIONS: The HLA alleles that occur with increased frequency in many HLA- associated conditions appear to serve as risk factors that increase susceptibility but are not essential for disease expression. Our data support the role of genetic factors in the development of HS, possibly related to early childhood events that may act as a trigger factor to initiate the cascade in genetically prone patients with specific HLA types to give rise to MTLE eventually.