scholarly journals Nutritional status of selenium in Alzheimer's disease patients

2009 ◽  
Vol 103 (6) ◽  
pp. 803-806 ◽  
Author(s):  
Bárbara Rita Cardoso ◽  
Thomas Prates Ong ◽  
Wilson Jacob-Filho ◽  
Omar Jaluul ◽  
Maria Isabel d'Ávila Freitas ◽  
...  

Studies have shown that various antioxidants are decreased in different age-related degenerative diseases and thus, oxidative stress would have a central role in the pathogenesis of many disorders that involve neuronal degeneration, including Alzheimer's disease (AD). The present study aimed to assess the nutritional status of Se in AD patients and to compare with control subjects with normal cognitive function. The case–control study was carried out on a group of elderly with AD (n 28) and compared with a control group (n 29), both aged between 60 and 89 years. Se intake was evaluated by using a 3-d dietary food record. Se was evaluated in plasma, erythrocytes and nails by using the method of hydride generation atomic absorption spectroscopy. Deficient Se intake was largely observed in the AD group. AD patients showed significantly lower Se levels in plasma, erythrocytes and nails (32·59 μg/l, 43·74 μg/l and 0·302 μg/g) when compared with the control group (50·99 μg/l, 79·16 μg/l and 0·400 μg/g). The results allowed us to suggest that AD has an important relation with Se deficiency.

F1000Research ◽  
2018 ◽  
Vol 7 ◽  
pp. 671
Author(s):  
Glaucia Renee Hilgemberg ◽  
Aline Jacoski de Oliveira Krüger da Silva ◽  
Bárbara Luisa Fermino ◽  
Camila Diedrich ◽  
Simone Carla Benincá ◽  
...  

Background: Alzheimer's disease (AD) is the most common cause of dementia, with a multifactorial etiology, in which the person has great difficulty identifying feelings of hunger, satiety, and feeding, which may affect their nutritional status. Pathologically, it is associated with neurodegeneration of synapses followed by neuronal loss, accompanied by glial proliferation surrounded by neurofibrillary tangles, beta-amyloid peptide (Aβ) deposition, inflammation and cerebrovascular injury hindering the ability to perform activities of daily living. This study aimed to analyze quantitatively the differences between an elderly group with AD and a control group, in terms of macro and micronutrient consumption evaluation. Methods: the study involved 69 participants who were assessed via collection of anthropometric measurements (weight, height and body mass index) with nutritional status being assessed by 24-hour food recall and three-day food record. Cognitive assessments were performed using the Mini-Mental State Examination (MMSE) and Clinical Dementia Ranting (CDR). Results: The intake of lipids in patients with severe dementia, was lower (p <0.05). The consumption of proteins showed a decrease with demential advance. For vitamins, there was a significant difference (p <0.05) in the amount of thiamine, niacin, vitamin D, E and K and calcium, chromium and iodine minerals, which were significantly reduced in AD patients (p <0.05). Conclusions: Decreases in macronutrient and micronutrient consumption may result in a consequent impairment of nutritional status, dementia progression, and decreased quality and life expectancy of elderly patients with AD.


2012 ◽  
Vol 18 (2) ◽  
pp. 191-199 ◽  
Author(s):  
Erika J. Laukka ◽  
Stuart W.S. MacDonald ◽  
Laura Fratiglioni ◽  
Lars Bäckman

AbstractWe investigated differences between Alzheimer's disease (AD) and vascular dementia (VaD) from the appearance of the first cognitive symptoms, focusing on both time of onset and rate of accelerated decline for different cognitive functions before dementia diagnosis. Data from a longitudinal population-based study were used, including 914 participants (mean age = 82.0 years, SD = 5.0) tested with a cognitive battery (word recall and recognition, Block Design, category fluency, clock reading) on up to four occasions spanning 10 years. We fit a series of linear mixed effects models with a change point to the cognitive data, contrasting each dementia group to a control group. Significant age-related decline was observed for all five cognitive tasks. Relative to time of diagnosis, the preclinical AD persons deviated from the normal aging curve earlier (up to 9 years) compared to the preclinical VaD persons (up to 6 years). However, once the preclinical VaD persons started to decline, they deteriorated at a faster rate than the preclinical AD persons. The results have important implications for identifying the two dementia disorders at an early stage and for selecting cognitive tasks to evaluate treatment effects for persons at risk of developing AD and VaD. (JINS, 2012, 18, 191–199)


2020 ◽  
Vol 22 (2) ◽  
Author(s):  
Amin Dehbozorgi ◽  
Laleh Behbudi Tabrizi ◽  
Seyed Ali Hosseini ◽  
Masod Haj Rasoli

Background: Alzheimer’s disease (AD) is an age-related neurodegenerative disorder. Evidence from neuropathological studies indicates that the levels of neurotrophins brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) are compromised in AD. Objectives: The present study aimed to review the effects of swimming training and royal jelly (RJ) on BDNF and NGF gene expression in the hippocampus tissue of rats with AD. Methods: In the present experimental study, 25 rats with AD were divided into five groups, including (1) control, (2) sham, (3) RJ, (4) training, and (5) training with RJ. Five healthy rats were selected as the healthy control group to examine the effect of AD induction by 8 mg/kg trimethyltin chloride (TMT) intra-peritoneally on BDNF and NGF. During eight weeks, groups 3 and 5 received 100 mg/kg RJ daily intra-peritoneally, and groups 4 and 5 swam in a rat swimming tank three sessions per week. One-way ANOVA with Tukey’s post hoc test was used for data analysis in SPSS 20 software (P < 0.05). Results: The induction of AD by TMT had a significant effect on the reduction of BDNF (P = 0.001) and NGF (P = 0.001). However, RJ had a significant effect on the increase of NGF (P = 0.03). Nevertheless, RJ (P = 0.99), training (P = 0.99), and training with RJ (P = 0.94) had no significant effect on BDNF and training (P = 0.99) and training with RJ (P = 0.97) had no significant effect on NGF. Conclusions: It appears that RJ has a significant effect on the increase of NGF gene expression in the hippocampus tissue of rats with AD. Nevertheless, RJ consumption simultaneously with swimming training has no significant effect on BDNF and NGF.


2018 ◽  
Vol 3 (3) ◽  
pp. e0303104
Author(s):  
Iryna Mudrenko

Background Dementia is the age-related disease. At the same time, the elderly age has one of the peaks in the number of suicides. Psychology of patients with demetia is characterized by the feeling of hopelessness, pessimism, awareness of own insolvency, dependence on others, that affects the risk of suicide. It is established that the highest risk of suicide in the early stages of dementia with the progression of cognitive deficit, the risk of suicide decreases. Aim To study the role of impairment of higher mental functions (perception, reasoning, attention, memory, emotions, will, speech) in the formation of suicidal behaviour in patients with dementia in Alzheimer's disease. Materials and methods There were examined 75 patients with dementia in Alzheimer's disease, 36 patients with a history of suicidal behavior composed the main group, and 39 patients without the signs of suicidal behavior composed control group. The study was carried out using clinical-anamnestic, psychopathological methods and mathematical statistical methods. Results The high risk of suicide in dementia caused by Alzheimer's disease is combined with the inhibition of thinking, the delusional ideas of self-blame and self-effacement (p ≤ 0.05); depressed mood, inner agitation, anxiety, feeling of despair, hopelessness, guilt, melancholia, apathy (p ≤ 0.05); effector-volitional disorders in the form of hypobulia, hypokinesia, hypomimia, decreased libido (p ≤ 0.05); speech disturbance in the form of bradylalia p ≤ 0.05; greater exhaustion and decreased attention (p ≤ 0.05). On the contrary, the following peculiarities of higher mental functions, namely thought disorder are referred to the anti-risk factors of suicide in dementia caused by Alzheimer's disease: the delusional ideas of relation and damage (p ≤ 0.05); emotions: the feeling of fear (p ≤ 0.05); effector-volitional sphere: parabulia and hyperkinesia (p ≤ 0.05). Conclusion On the basis of clinical and psychopathological study of patients with dementia in Alzheimer's disease, the specific impairment of higher mental functions and emotional-volitional spheres reasoning, memory, attention, perception, speech, emotions) are identified associated with high risk of suicide.


2020 ◽  
Vol 13 (2) ◽  
pp. 102-112
Author(s):  
Zois Papadopoulos

: In developed countries, people of advanced age go permanently blind most often due to age-related macular degeneration, while at the global level, this disease is the third major cause of blindness, after cataract and glaucoma, according to the World Health Organisation. The number of individuals believed to suffer from the disease throughout the world has been approximated at 50 million. Age-related macular degeneration is classified as non-neovascular (dry, non-exudative) and neovascular (wet, exudative). The exudative form is less common than the non-exudative as it accounts for approximately 10 percent of the cases of the disease. However, it can be much more aggressive and could result in a rapid and severe loss of central vision. Similarly, with age-related macular degeneration, Alzheimer’s disease is a late-onset, neurodegenerative disease affecting millions of people worldwide. Both of them are associated with age and share several features, including the presence of abnormal extracellular deposits associated with neuronal degeneration, drusen, and plaques, respectively. The present review article highlights the pathogenesis, clinical features, and imaging modalities used for the diagnosis of neovascular age-related macular degeneration. A thorough overview of the effectiveness of anti-VEGF agents as well as of other treatment modalities that have either lost favour or, are rarely used, is provided in detail. Additionally, the common histologic, immunologic, and pathogenetic features of Alzheimer’s disease and age-related macular degeneration are discussed in depth.


1999 ◽  
Vol 11 (4) ◽  
pp. 227-231 ◽  
Author(s):  
T. Vecchi ◽  
V. Saveriano ◽  
L. Paciaroni

A selective deterioration of working memory functions has been suggested as an explanation of the cognitive decay occurring in normal ageing as well as in Alzheimer-type dementia. Recent studies have highlighted that elderly people’s limitations in working memory functions may be better interpreted when analysing the specific characteristics of the cognitive process (i.e., passive storage or active manipulation of information). In the present study, we have adapted a procedure used to investigate age-related memory modifications, involving both verbal and visuo-spatial material in tasks tapping passive and active processes, to investigate the deterioration associated with Alzheimer's disease. A group of Alzheimer patients in the early stages of the disease were matched to a control group of healthy elderly. Results show that Alzheimer patients performed less accurately than the control group in all tasks. However, the deficit was maximised in the case of active processes, regardless of the type of material used (verbal or visuo-spatial). These data highlight the importance of considering the amount of active processing as the key variable when interpreting the decay in cognitive functions in the early stages of Alzheimer’s disease.


2000 ◽  
Vol 9 (5) ◽  
pp. 629-636 ◽  
Author(s):  
Mark H. Tuszynski

Nerve growth factor (NGF) exerts both trophic (cell survival) and tropic (axonal growth-promoting) effects on several neuronal populations. In particular, its robust ability to prevent lesion-induced and spontaneous age-related basal forebrain cholinergic neuronal degeneration, and to promote mnemonic recovery, has suggested its potential use as a therapeutic agent in Alzheimer's disease. When infused intracerebroventricularly, however, NGF is associated with several adverse effects that make this delivery route impractical. The present study examined whether intraparenchymal infusions of NGF adjacent to cholinergic neuronal soma are an effective and well-tolerated means of providing NGF to degenerating cholinergic neurons. Cholinergic neuronal rescue together with axonal sprouting responses and local tissue damage in the brain were assessed in adult rats that underwent complete unilateral fornix transections, followed by intraparenchymal infusions of recombinant human NGF for a 2-week period. Intraparenchymal NGF infusions prevented the degeneration of 94.7 ± 6.6% of basal forebrain cholinergic neurons compared to 21.7 ± 2.6% in vehicle-infused animals (p < 0.0001). Cholinergic axons sprouted toward the intraparenchymal NGF source in an apparent gradient-dependent manner. Glial responses to intraparenchymal infusions were minimal, and no apparent toxic effects of the infusions were observed. Thus, when infused intraparenchymally, NGF rescues basal forebrain cholinergic neurons, alters the topography of axonal sprouting responses, and does not induce adverse affects over a 2-week infusion period. Intraparenchymal NGF delivery merits further study at longer term time points as a means of treating the cholinergic component of neuronal loss in Alzheimer's disease.


2017 ◽  
Vol 29 (8) ◽  
pp. 1355-1361 ◽  
Author(s):  
N. A. Arnaoutoglou ◽  
M. Arnaoutoglou ◽  
P. Nemtsas ◽  
V. Costa ◽  
S. J. Baloyannis ◽  
...  

ABSTRACTBackground:Alzheimer's Disease (AD) and Vascular Dementia (VaD) are the most common causes of dementia in older people. Both diseases appear to have similar clinical symptoms, such as deficits in attention and executive function, but specific cognitive domains are affected. Current cohort studies have shown a close relationship between αβ deposits and age-related macular degeneration (Johnson et al., 2002; Ratnayaka et al., 2015). Additionally, a close link between the thinning of the retinal nerve fiber (RNFL) and AD patients has been described, while it has been proposed that AD patients suffer from a non-specific type of color blindness (Pache et al., 2003).Methods:Our study included 103 individuals divided into three groups: A healthy control group (n = 35), AD (n = 32) according to DSM-IV-TR, NINCDS-ADRDA criteria, and VaD (n = 36) based on ΝΙΝDS-AIREN, as well as Magnetic Resonance Imaging (MRI) results. The severity of patient's cognitive impairment, was measured with the Mini-Mental State Examination (MMSE) and was classified according to the Reisberg global deterioration scale (GDS). Visual perception was examined using the Ishihara plates: “Ishihara Color Vision Test - 38 Plate.”Results:The three groups were not statistically different for demographic data (age, gender, and education). The Ishihara color blindness test has a sensitivity of 80.6% and a specificity of 87.5% to discriminate AD and VaD patients when an optimal (32.5) cut-off value of performance is used.Conclusions:Ishihara Color Vision Test - 38 Plate is a promising potential method as an easy and not time-consuming screening test for the differential diagnosis of dementia between AD and VaD.


1997 ◽  
Vol 77 (4) ◽  
pp. 1081-1132 ◽  
Author(s):  
M. P. Mattson

beta-Amyloid precursor protein (beta-APP), the source of the fibrillogenic amyloid beta-peptide (A beta) that accumulates in the brain of victims of Alzheimer's disease, is a multifunctional protein that is widely expressed in the nervous system. beta-Amyloid precursor protein is axonally transported and accumulates in presynaptic terminals and growth cones. A secreted form of beta-APP (sAPP alpha) is released from neurons in response to electrical activity and may function in modulation of neuronal excitability, synaptic plasticity, neurite outgrowth, synaptogenesis, and cell survival. A signaling pathway involving guanosine 3',5'-cyclic monophosphate is activated by sAPP alpha and modulates the activities of potassium channels, N-methyl-D-aspartate receptors, and the transcription factor NF kappa B. Additional functions of beta-APP may include modulation of cell adhesion and regulation of proliferation of nonneuronal cells. Alternative enzymatic processing of beta-APP liberates A beta, which has a propensity to form amyloid fibrils; A beta can damage and kill neurons and increase their vulnerability to excitotoxicity. The mechanism involves generation of oxyradicals and impairment of membrane transport systems (e.g., ion-motive ATPases and glutamate and glucose transporters). Genetic mutations or age-related metabolic changes may promote neuronal degeneration in Alzheimer's disease by increasing production of A beta and/or decreasing levels of neuroprotective sAPP alpha.


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