scholarly journals Young Coconut Juice Reduces Some Histopathological Changes Associated with Alzheimer’s Disease through the Modulation of Estrogen Receptors in Orchidectomized Rat Brains

2019 ◽  
Vol 2019 ◽  
pp. 1-14
Author(s):  
Tatcha Balit ◽  
Mosaad A. Abdel-Wahhab ◽  
Nisaudah Radenahmad
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Estrogen Receptors ◽  
Estradiol Benzoate ◽  
Protective Role ◽  
Control Group ◽  
Amyloid A ◽  
Estrogen Receptor Modulators ◽  
End Of Treatment ◽  
The Brain

Propose. This study aimed to evaluate the protective role of young coconut juice (YCJ) against the pathological changes in Alzheimer’s disease (AD) in orchidectomized (orx) rats. Methods and Results. Animals were divided into 7 groups including: baseline normal control group, sham control, orx rat group, orx rat group injected with 2.5 μg/kg b.w. estradiol benzoate (EB) 3 days a week for 10 weeks, and the orx rat groups treated orally with 10, 20, and 40 ml/kg b.w. of YCJ for 10 weeks. At the end of treatment period, animals were sacrificed and the brain of each rat was removed, fixed in 10% neutral formalin, and stained by specific antibodies against NF200, parvalbumin (PV), β-amyloid (Aβ), and estrogen receptors (ERα and ERβ). The results showed that the number of NF200- and PV-reactive neurons in the hippocampus and cerebral cortex was significantly reduced in orx rats. However, it restored to normal in orx rats injected with EB or those administrated with YCJ in a dose-related manner. Neurons containing β-amyloid (Aβ), a hallmark of Alzheimer’s disease (AD), were found to be increased in the orx rats; however; they were reduced by EB injection or YCJ administration. These results suggested the binding of the YCJ active ingredient(s) with estrogen receptors (ERs) in the brain as indicated by the detection of ERα and ERβ in neurons since a significant correlation was detected between NF200-/PV-reactive neurons vs ERα-/ERβ-reactive neurons.Conclusion. It could be concluded that YCJ is effective as EB in reducing AD pathology, probably by being selective estrogen receptor modulators.

scholarly journals Genetic Variants of Lipoprotein Lipase and Regulatory Factors Associated with Alzheimer’s Disease Risk

2020 ◽  
Vol 21 (21) ◽  
pp. 8338
Author(s):  
Kimberley D. Bruce ◽  
Maoping Tang ◽  
Philip Reigan ◽  
Robert H. Eckel
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Lipoprotein Lipase ◽  
Genetic Variants ◽  
Disease Risk ◽  
Lipoprotein Metabolism ◽  
Protective Role ◽  
Direct Role ◽  
The Brain

Lipoprotein lipase (LPL) is a key enzyme in lipid and lipoprotein metabolism. The canonical role of LPL involves the hydrolysis of triglyceride-rich lipoproteins for the provision of FFAs to metabolic tissues. However, LPL may also contribute to lipoprotein uptake by acting as a molecular bridge between lipoproteins and cell surface receptors. Recent studies have shown that LPL is abundantly expressed in the brain and predominantly expressed in the macrophages and microglia of the human and murine brain. Moreover, recent findings suggest that LPL plays a direct role in microglial function, metabolism, and phagocytosis of extracellular factors such as amyloid- beta (Aβ). Although the precise function of LPL in the brain remains to be determined, several studies have implicated LPL variants in Alzheimer’s disease (AD) risk. For example, while mutations shown to have a deleterious effect on LPL function and expression (e.g., N291S, HindIII, and PvuII) have been associated with increased AD risk, a mutation associated with increased bridging function (S447X) may be protective against AD. Recent studies have also shown that genetic variants in endogenous LPL activators (ApoC-II) and inhibitors (ApoC-III) can increase and decrease AD risk, respectively, consistent with the notion that LPL may play a protective role in AD pathogenesis. Here, we review recent advances in our understanding of LPL structure and function, which largely point to a protective role of functional LPL in AD neuropathogenesis.

scholarly journals Tau-Reactive Endogenous Antibodies: Origin, Functionality, and Implications for the Pathophysiology of Alzheimer’s Disease

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Lenka Hromadkova ◽  
Saak Victor Ovsepian
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Critical Evaluation ◽  
Circulatory System ◽  
Peripheral Circulation ◽  
Protective Role ◽  
Tau Pathology ◽  
Systematic Analysis ◽  
Neurodegenerative Process ◽  
The Brain

In Alzheimer’s disease (AD), tau pathology manifested in the accumulation of intraneuronal tangles and soluble toxic oligomers emerges as a potential therapeutic target. Multiple anti-tau antibodies inhibiting the formation and propagation of cytotoxic tau or promoting its clearance and degradation have been tested in clinical trials, albeit with the inconclusive outcome. Antibodies against tau protein have been found both in the brain circulatory system and at the periphery, but their origin and role under normal conditions and in AD remain unclear. While it is tempting to assign them a protective role in regulating tau level and removal of toxic variants, the supportive evidence remains sporadic, requiring systematic analysis and critical evaluation. Herein, we review recent data showing the occurrence of tau-reactive antibodies in the brain and peripheral circulation and discuss their origin and significance in tau clearance. Based on the emerging evidence, we cautiously propose that impairments of tau clearance at the periphery by humoral immunity might aggravate the tau pathology in the central nervous system, with implication for the neurodegenerative process of AD.

scholarly journals Spatial analysis of thickness changes in ten retinal layers of Alzheimer’s disease patients based on optical coherence tomography

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Luis Jáñez-Escalada ◽  
Lucía Jáñez-García ◽  
Elena Salobrar-García ◽  
Alejandro Santos-Mayo ◽  
Rosa de Hoz ◽  
...  
Keyword(s):  
Field Theory ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Outer Segment ◽  
Control Group ◽  
Random Field Theory ◽  
Retinal Layers ◽  
Outer Segments ◽  
The Mean ◽  
The Brain

Abstract The retina is an attractive source of biomarkers since it shares many features with the brain. Thickness differences in 10 retinal layers between 19 patients with mild Alzheimer’s disease (AD) and a control group of 24 volunteers were investigated. Retinal layers were automatically segmented and their thickness at each scanned point was measured, corrected for tilt and spatially normalized. When the mean thickness of entire layers was compared between patients and controls, only the outer segment layer of patients showed statistically significant thinning. However, when the layers were compared point-by point, patients showed statistically significant thinning in irregular regions of total retina and nerve fiber, ganglion cell, inner plexiform, inner nuclear and outer segment layers. Our method, based on random field theory, provides a precise delimitation of regions where total retina and each of its layers show a statistically significant thinning in AD patients. All layers, except inner nuclear and outer segments, showed thickened regions. New analytic methods have shown that thinned regions are interspersed with thickened ones in all layers, except inner nuclear and outer segments. Across different layers we found a statistically significant trend of the thinned regions to overlap and of the thickened ones to avoid overlapping.

scholarly journals P-glycoprotein (ABCB1) and Oxidative Stress: Focus on Alzheimer’s Disease

2017 ◽  
Vol 2017 ◽  
pp. 1-13 ◽  
Author(s):  
Giulia Sita ◽  
Patrizia Hrelia ◽  
Andrea Tarozzi ◽  
Fabiana Morroni
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Therapeutic Drug ◽  
Amyloid A ◽  
P Glycoprotein ◽  
And Function ◽  
The Brain ◽  
Brain Homeostasis

ATP-binding cassette (ABC) transporters, in particular P-glycoprotein (encoded by ABCB1), are important and selective elements of the blood-brain barrier (BBB), and they actively contribute to brain homeostasis. Changes in ABCB1 expression and/or function at the BBB may not only alter the expression and function of other molecules at the BBB but also affect brain environment. Over the last decade, a number of reports have shown that ABCB1 actively mediates the transport of beta amyloid (Aβ) peptide. This finding has opened up an entirely new line of research in the field of Alzheimer’s disease (AD). Indeed, despite intense research efforts, AD remains an unsolved pathology and effective therapies are still unavailable. Here, we review the crucial role of ABCB1 in the Aβtransport and how oxidative stress may interfere with this process. A detailed understanding of ABCB1 regulation can provide the basis for improved neuroprotection in AD and also enhanced therapeutic drug delivery to the brain.

scholarly journals KL-VS heterozygosity is associated with lower amyloid-dependent tau accumulation and memory impairment in Alzheimer’s disease

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Julia Neitzel ◽  
Nicolai Franzmeier ◽  
Anna Rubinski ◽  
Martin Dichgans ◽  
Matthias Brendel ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Brain Regions ◽  
Protective Role ◽  
Amyloid Pet ◽  
Tau Pathology ◽  
Cross Sectional ◽  
Memory Impairments ◽  
Amyloid A ◽  
Tau Pet

AbstractKlotho-VS heterozygosity (KL-VShet) is associated with reduced risk of Alzheimer’s disease (AD). However, whether KL-VShet is associated with lower levels of pathologic tau, i.e., the key AD pathology driving neurodegeneration and cognitive decline, is unknown. Here, we assessed the interaction between KL-VShet and levels of beta-amyloid, a key driver of tau pathology, on the levels of PET-assessed neurofibrillary tau in 551 controls and patients across the AD continuum. KL-VShet showed lower cross-sectional and longitudinal increase in tau-PET per unit increase in amyloid-PET when compared to that of non-carriers. This association of KL-VShet on tau-PET was stronger in Klotho mRNA-expressing brain regions mapped onto a gene expression atlas. KL-VShet was related to better memory functions in amyloid-positive participants and this association was mediated by lower tau-PET. Amyloid-PET levels did not differ between KL-VShet carriers versus non-carriers. Together, our findings provide evidence to suggest a protective role of KL-VShet against amyloid-related tau pathology and tau-related memory impairments in elderly humans at risk of AD dementia.

scholarly journals Electroacupuncture Improves Clearance of Amyloid-β through the Glymphatic System in the SAMP8 Mouse Model of Alzheimer’s Disease

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Pei-zhe Liang ◽  
Li Li ◽  
Ya-nan Zhang ◽  
Yan Shen ◽  
Li-li Zhang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Neurodegenerative Disorder ◽  
Amyloid Β ◽  
Control Group ◽  
Nissl Staining ◽  
Glymphatic System ◽  
Model Of Alzheimer’S Disease ◽  
The Brain

Background. Memory loss and cognitive impairment characterize the neurodegenerative disorder, Alzheimer’s disease (AD). Amyloid-β (Aβ) is the key factor that triggers the course of AD, and reducing the deposition of Aβ in the brain has been considered as a potential target for the treatment of AD. In clinical and animal studies, electroacupuncture (EA) has been shown to be an effective treatment for AD. In recent years, substantial evidence has accumulated suggesting the important role of the glymphatic system in Aβ clearance. Objective. The purpose of this study was to explore whether EA modifies the accumulation of Aβ through the glymphatic system and may thus be applied to alleviate cognitive impairments. Methods. Seven-month-old SAMP8 mice were randomized into a control group (Pc) and an electroacupuncture group (Pe). Age-matched SAMR1 mice were used as normal controls (Rc). Mice in the Pe group were stimulated on Baihui (GV20) and Yintang (GV29) for 10 min and then pricked at Shuigou (GV26) for ten times. EA treatment lasted for 8 weeks. In each week, EA would be applied once a day for the first five consecutive days and ceased at the remaining two days. After EA treatment, Morris water maze (MWM) test was used to evaluate the cognitive function; HE and Nissl staining was performed to observe the brain histomorphology; ELISA, contrast-enhanced MRI, and immunofluorescence were applied to explore the mechanisms underlying EA effects from Aβ accumulation, glymphatic system function, reactivity of astrocytes, and AQP4 polarization, respectively. Results. This EA regime could improve cognition and alleviate neuropathological damage to brain tissue. And EA treatment might reduce Aβ accumulation, enhance paravascular influx in the glymphatic system, inhibit the reactivity of astrocytes, and improve AQP4 polarity. Conclusion. EA treatment might reduce Aβ accumulation from the brain via improving clearance performance of the glymphatic system and thereby alleviating cognitive impairment.

CT features of atrophy of the brain temporal lobes characteristic for Alzheimer’s disease with different stages of dementia

2011 ◽  
Vol 26 (S2) ◽  
pp. 941-941
Author(s):  
I.V. Maksimovich
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Control Group ◽  
Study Group ◽  
List Type ◽  
Type Number ◽  
Severe Dementia ◽  
Temporal Lobes ◽  
Clinical Stages ◽  
The Brain

BackgroundWhile diagnosing Alzheimer’s disease, there appear certain difficulties in the correlation of cerebral atrophy and the patient's clinical status.Methods93 patients were examined.Study group - 42 patients aged 34-79 with preclinical and clinical stages of Alzheimer’s disease:(1)- patients with high risk of acquiring the disease (those suffering from impaired memory, without any manifestations of dementia, whose 2 or more immediate relatives suffered from Alzheimer’s disease) 6 patients(2)- patients with mild dementia 14(3)- patients with moderate dementia 15(4)- patients with severe dementia 7Control group - 51 patients aged 28–78 with various kinds of brain lesions accompanied by dementia but not suffering from Alzheimer’s disease:-chronic cerebrovascular insufficiency 21 patients-severe vascular dementia 6-atherosclerotic parkinsonism 14-Binswanger’s disease 6-Parkinson’s disease 4ResultsIn Study group 1, 4 (66.6%) patients showed decrease of 4–8% in the size of the brain temporal lobes.In Study group 2, 14 (100%) patients showed decrease of 9–18%.In Study group 3, 15 (100%) patients showed decrease of 19–32%.In Study group 4, 7 (100%) patients showed decrease of 33–62%.Control group patients had no similar changes in the temporal lobes.ConclusionsStructural and morphological changes of the brain characteristic for Alzheimer’s disease are atrophy of the temporal lobes and hippocampus which makes 4–8% in pre-clinical stages of the disease, 9–18% in mild, 19–32% in moderate and 33–62% in severe dementia.

scholarly journals Easy Identification of Optimal Coronal Slice on Brain Magnetic Resonance Imaging to Measure Hippocampal Area in Alzheimer’s Disease Patients

2020 ◽  
Vol 2020 ◽  
pp. 1-6
Author(s):  
P. Zach ◽  
A. Bartoš ◽  
A. Lagutina ◽  
Z. Wurst ◽  
P. Gallina ◽  
...  
Keyword(s):  
Magnetic Resonance Imaging ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Magnetic Resonance ◽  
Brain Magnetic Resonance Imaging ◽  
Control Group ◽  
Resonance Imaging ◽  
Hippocampal Area ◽  
Left And Right ◽  
The Brain

Introduction. Measurement of an- hippocampal area or volume is useful in clinical practice as a supportive aid for diagnosis of Alzheimer’s disease. Since it is time-consuming and not simple, it is not being used very often. We present a simplified protocol for hippocampal atrophy evaluation based on a single optimal slice in Alzheimer’s disease. Methods. We defined a single optimal slice for hippocampal measurement on brain magnetic resonance imaging (MRI) at the plane where the amygdala disappears and only the hippocampus is present. We compared an absolute area and volume of the hippocampus on this optimal slice between 40 patients with Alzheimer disease and 40 age-, education- and gender-mateched elderly controls. Furthermore, we compared these results with those relative to the size of the brain or the skull: the area of the optimal slice normalized to the area of the brain at anterior commissure and the volume of the hippocampus normalized to the total intracranial volume. Results. Hippocampal areas on the single optimal slice and hippocampal volumes on the left and right in the control group were significantly higher than those in the AD group. Normalized hippocampal areas and volumes on the left and right in the control group were significantly higher compared to the AD group. Absolute hippocampal areas and volumes did not significantly differ from corresponding normalized hippocampal areas as well as normalized hippocampal volumes using comparisons of areas under the receiver operating characteristic curves. Conclusion. The hippocampal area on the well-defined optimal slice of brain MRI can reliably substitute a complicated measurement of the hippocampal volume. Surprisingly, brain or skull normalization of these variables does not add any incremental differentiation between Alzheimer disease patients and controls or give better results.

scholarly journals KL-VS heterozygosity is associated with reduced tau accumulation and lower memory impairment in Alzheimer's disease

2020 ◽  
Author(s):  
Julia Neitzel ◽  
Nicolai Franzmeier ◽  
Anna Rubinski ◽  
Martin Dichgans ◽  
Matthias Brendel ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Brain Regions ◽  
Protective Role ◽  
Amyloid Pet ◽  
Tau Pathology ◽  
Cross Sectional ◽  
Memory Impairments ◽  
Amyloid A ◽  
Tau Pet

Klotho-VS heterozygosity (KL-VShet) is associated with reduced risk of Alzheimer's disease (AD). However, whether KL-VShet is associated with lower levels of pathologic tau, i.e. the key AD pathology driving neurodegeneration and cognitive decline, is unknown. Here, we assessed the interaction between KL-VShet and levels of beta-amyloid, a key driver of tau pathology, on the levels of PET-assessed neurofibrillary tau in 354 controls and patients within the AD continuum. KL-VShet showed lower cross-sectional increase in tau-PET per unit increase in amyloid-PET when compared to that of non-carriers. This effect of KL-VShet on tau-PET showed a tendency to be stronger in Klotho mRNA-expressing brain regions mapped onto a gene expression atlas. KL-VShet was related to better memory functions and this association was mediated by lower tau-PET. Amyloid-PET levels did not differ between KL-VShet carriers versus non-carriers. Together, our findings provide evidence for a protective role of KL-VShet against tau pathology and tau-related memory impairments in elderly humans at risk of AD dementia.

scholarly journals Influence of PICALM and CLU risk variants on beta EEG activity in Alzheimer’s disease patients

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Aarón Maturana-Candelas ◽  
Carlos Gómez ◽  
Jesús Poza ◽  
Víctor Rodríguez-González ◽  
Vìctor Gutiérrez-de Pablo ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Regional Distribution ◽  
Control Group ◽  
Protective Effects ◽  
Beta Band ◽  
Eeg Activity ◽  
Spatial Entropy ◽  
Beta Power ◽  
The Brain

AbstractPICALM and CLU genes have been linked to alterations in brain biochemical processes that may have an impact on Alzheimer’s disease (AD) development and neurophysiological dynamics. The aim of this study is to analyze the relationship between the electroencephalographic (EEG) activity and the PICALM and CLU alleles described as conferring risk or protective effects on AD patients and healthy controls. For this purpose, EEG activity was acquired from: 18 AD patients and 12 controls carrying risk alleles of both PICALM and CLU genes, and 35 AD patients and 12 controls carrying both protective alleles. Relative power (RP) in the conventional EEG frequency bands (delta, theta, alpha, beta, and gamma) was computed to quantify the brain activity at source level. In addition, spatial entropy (SE) was calculated in each band to characterize the regional distribution of the RP values throughout the brain. Statistically significant differences in global RP and SE at beta band (p-values < 0.05, Mann–Whitney U-test) were found between genotypes in the AD group. Furthermore, RP showed statistically significant differences in 58 cortical regions out of the 68 analyzed in AD. No statistically significant differences were found in the control group at any frequency band. Our results suggest that PICALM and CLU AD-inducing genotypes are involved in physiological processes related to disruption in beta power, which may be associated with physiological disturbances such as alterations in beta-amyloid and neurotransmitter metabolism.

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