scholarly journals Therapeutic Plasmapheresis with Albumin Replacement in Alzheimer’s Disease and Chronic Progressive Multiple Sclerosis: A Review

2020 ◽  
Vol 13 (2) ◽  
pp. 28 ◽  
Author(s):  
Rut Navarro-Martínez ◽  
Omar Cauli
Keyword(s):  
Multiple Sclerosis ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Clinical Symptoms ◽  
Alternative Therapy ◽  
Progressive Multiple Sclerosis ◽  
Neurological Deficits ◽  
Chronic Progressive Multiple Sclerosis ◽  
Progressive Form ◽  
The Brain

Background: Reducing the burden of beta-amyloid accumulation and toxic autoimmunity-related proteins, one of the recognized pathophysiological markers of chronic and common neurological disorders such as Alzheimer’s disease (AD) and multiple sclerosis (MS), may be a valid alternative therapy to reduce their accumulation in the brain and thus reduce the progression of these disorders. The objective of this review was to evaluate the efficacy of plasmapheresis (PP) in AD and chronic progressive MS patients (in terms of improving clinical symptoms) and to analyze its safety and protocols. Methods: Articles related to this topic and published without time limitations in the Medline, and Cochrane databases were reviewed. Results: In AD patients, PP reduced amyloid beta (Aβ) levels in the brain, accompanied by a tendency towards cognitive stabilization, and improved language and verbal fluency. In regards to structural and functional brain changes, PP reduced brain volume and favored the stabilization, or absence, of the progression of perfusion. In chronic progressive form of MS patients, PP improved neurological deficits in 20–70% of patients with a chronic progressive form of MS, and restored interferon (IFN) responsiveness, which was not accompanied by any image change in brain plaques. Conclusions: Therapeutic plasmapheresis with albumin replacement is a promising strategy for reducing Aβ mediated toxicity and slowing the progression of the disorder. Some patients with chronic progressive forms of MS show improvement in neurological deficits. The features of AD and MS patients who benefit most from this approach need further research.

MR Brain Screening using Optimization Techniques – A survey

2021 ◽  
Vol 17 ◽  
Author(s):  
Chitradevi D ◽  
Prabha S.
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Clinical Symptoms ◽  
Memory Loss ◽  
Amyloid Β ◽  
Cell Loss ◽  
Optimization Techniques ◽  
Amyloid Β Protein ◽  
The Brain ◽  
Brain Tissues

Background: Alzheimer’s disease (AD) is associated with Dementia, and it is also a memory syndrome in the brain. It affects the brain tissues and causes major changes in day-to-day activities. Aging is a major cause of Alzheimer's disease. AD is characterized by two pathological hallmarks as, Amyloid β protein and neurofibrillary tangles of hyperphosphorylated tau protein. The imaging hallmarks for Alzheimer’s disease are namely, swelling, shrinkage of brain tissues due to cell loss, and atrophy in the brain due to protein dissemination. Based on the survey, 60% to 80% of dementia patients belong to Alzheimer’s disease. Introduction: AD is now becoming an increasing and important brain disease. The goal of AD pathology is to cause changes/damage in brain tissues. Alzheimer's disease is thought to begin 20 years or more before symptoms appear, with tiny changes in the brain that are undetectable to the person affected. The changes in a person's brain after a few years are noticeable through symptoms such as language difficulties and memory loss. Neurons in different parts of the brain have detected symptoms such as cognitive impairments and learning disabilities. In this case, neuroimaging tools are necessary to identify the development of pathology which relates to the clinical symptoms. Methods: Several approaches have been tried during the last two decades for brain screening to analyse AD with the process of pre-processing, segmentation and classification. Different individual such as Grey Wolf optimization, Lion Optimization, Ant Lion Optimization and so on. Similarly, hybrid optimization techniques are also attempted to segment the brain sub-regions which helps in identifying the bio-markers to analyse AD. Conclusion: This study discusses a review of neuroimaging technologies for diagnosing Alzheimer's disease, as well as the discovery of hallmarks for the disease and the methodologies for finding hallmarks from brain images to evaluate AD. According to the literature review, most of the techniques predicted higher accuracy (more than 90%), which is beneficial for assessing and screening neurodegenerative illness, particularly Alzheimer's disease.

scholarly journals A Systematic Review of Glucose Transport Alterations in Alzheimer's Disease

2021 ◽  
Vol 15 ◽  
Author(s):  
Natalia Kyrtata ◽  
Hedley C. A. Emsley ◽  
Oli Sparasci ◽  
Laura M. Parkes ◽  
Ben R. Dickie
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Glucose Transport ◽  
Clinical Symptoms ◽  
Amyloid Β ◽  
Neuronal Cell ◽  
Glucose Transporters ◽  
Rodent Models ◽  
The Brain

Introduction: Alzheimer's disease (AD) is characterized by cerebral glucose hypometabolism. Hypometabolism may be partly due to reduced glucose transport at the blood-brain barrier (BBB) and across astrocytic and neuronal cell membranes. Glucose transporters (GLUTs) are integral membrane proteins responsible for moving glucose from the bloodstream to parenchymal cells where it is metabolized, and evidence indicates vascular and non-vascular GLUTs are altered in AD brains, a process which could starve the brain of glucose and accelerate cognitive decline. Here we review the literature on glucose transport alterations in AD from human and rodent studies.Methods: Literature published between 1st January 1946 and 1st November 2020 within EMBASE and MEDLINE databases was searched for the terms “glucose transporters” AND “Alzheimer's disease”. Human and rodent studies were included while reviews, letters, and in-vitro studies were excluded.Results: Forty-three studies fitting the inclusion criteria were identified, covering human (23 studies) and rodent (20 studies). Post-mortem studies showed consistent reductions in GLUT1 and GLUT3 in the hippocampus and cortex of AD brains, areas of the brain closely associated with AD pathology. Tracer studies in rodent models of AD and human AD also exhibit reduced uptake of glucose and glucose-analogs into the brain, supporting these findings. Longitudinal rodent studies clearly indicate that changes in GLUT1 and GLUT3 only occur after amyloid-β pathology is present, and several studies indicate amyloid-β itself may be responsible for GLUT changes. Furthermore, evidence from human and rodent studies suggest GLUT depletion has severe effects on brain function. A small number of studies show GLUT2 and GLUT12 are increased in AD. Anti-diabetic medications improved glucose transport capacity in AD subjects.Conclusions: GLUT1 and GLUT3 are reduced in hippocampal and cortical regions in patients and rodent models of AD, and may be caused by high levels of amyloid-β in these regions. GLUT3 reductions appear to precede the onset of clinical symptoms. GLUT2 and GLUT12 appear to increase and may have a compensatory role. Repurposing anti-diabetic drugs to modify glucose transport shows promising results in human studies of AD.

scholarly journals Disorders of cognitive activity in patients with multiple sclerosis and hepatocerebral degeneration and its prevention

2020 ◽  
Vol 24 (4) ◽  
pp. 589-594
Author(s):  
I. Voloshyn-Gaponov ◽  
I. Lantukh ◽  
P. Gaponov
Keyword(s):  
Multiple Sclerosis ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Functions ◽  
Verbal Memory ◽  
Cognitive Activity ◽  
Cognitive Disorders ◽  
Biological Aging ◽  
Treatment And Prevention ◽  
The Brain

Annotation. Currently, there is an increase in dementias of various origins, which is largely due to the tendency of the aging population of the globe, with adverse environmental factors. Dementia also occurs at a young, working-aged, which makes them not only a medical but also a social problem. The incidence of Alzheimer's disease (AD) is so high that the WHO has declared the 21st century the century of the AD epidemic. The task of the work is to conduct a comprehensive clinical and laboratory examination of patients with multiple sclerosis (MS) and patients with Wilson's disease (WD) to study the problem of neurodegenerative diseases. The Mini-Mental Status Exam (MMSE) scale was used to screen for cognitive function and to study the level of intellectual performance of patients. To determine verbal memory, the method was used: “memorization of 10 words”, and to study the personality and emotional sphere, the method of Derogatis SCl-90-P was used. The sample of patients with MS was 111 people, and psycho diagnostic examination of patients with WD was performed in 33 patients. Various cognitive disorders are characteristic of MS patients. The level of general intellectual productivity is in the range from normative indicators to very pronounced systemic disorders of cognitive functions. With the age of patients and the duration of the disease, the severity of these disorders increases. A comprehensive clinical and laboratory study showed that the pathogenesis and stages of development of the dementia process in patients with WD and MS coincide with those in patients with Alzheimer’s disease and depends on three groups of factors: genetic predisposition, natural (biological) aging, and endogenous and exogenous pathogenic factors. on the brain. The study concluded that in patients with WD and MS in the pathogenetic process are always involved structures that ensure the functioning of cognitive functions of the brain, which leads to the development of their defects. For the treatment and prevention of these patients, a comprehensive, pathogenetically grounded, and personalized therapy should be prescribed.

scholarly journals Fiber Tracts Anomalies in APPxPS1 Transgenic Mice Modeling Alzheimer's Disease

2011 ◽  
Vol 2011 ◽  
pp. 1-12 ◽  
Author(s):  
H. Chen ◽  
S. Epelbaum ◽  
B. Delatour
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transgenic Mice ◽  
Clinical Symptoms ◽  
Anterior Commissure ◽  
Fiber Tract ◽  
Fiber Tracts ◽  
Age Related ◽  
The Impact ◽  
The Brain

Amyloid beta (A) peptides are known to accumulate in the brain of patients with Alzheimer's disease (AD). However, the link between brain amyloidosis and clinical symptoms has not been elucidated and could be mediated by secondary neuropathological alterations such as fiber tracts anomalies. In the present study, we have investigated the impact of A overproduction in APPxPS1 transgenic mice on the integrity of forebrain axonal bundles (corpus callosum and anterior commissure). We found evidence of fiber tract volume reductions in APPxPS1 mice that were associated with an accelerated age-related loss of axonal neurofilaments and a myelin breakdown. The severity of these defects was neither correlated with the density of amyloid plaques nor associated with cell neurodegeneration. Our data suggest that commissural fiber tract alterations are present in A-overproducing transgenic mice and that intracellular A accumulation preceding extracellular deposits may act as a trigger of such morphological anomalies.

scholarly journals Comparison of Tractography in Mouse Models of Multiple Sclerosis and Alzheimer’s Disease

2017 ◽  
Vol 3 (1) ◽  
pp. 37-46
Author(s):  
Winnica Beltrano ◽  
Zoe O’Brien-Moran ◽  
Sheryl L Herrera ◽  
Melanie Martin
Keyword(s):  
Multiple Sclerosis ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Mouse Models ◽  
Wildtype Mouse ◽  
Analysis Method ◽  
Fiber Tracts ◽  
Model Of Alzheimer’S Disease ◽  
The Brain

Tractography is a method that finds fiber tracts within a sample (e.g. a mouse brain), which allows users to better understand how different regions and structures of the brain are connected. The only animal magnetic resonance imaging (MRI) centre in Manitoba does not have the software to perform tractography on their images. This severely limits the variation of studies that can be performed in the centre. The goal of this project was to develop a robust tractography analysis method for the centre. The designed tractography analysis method was tested on known phantoms (objects which are meant to mimic tissue) such as celery, and then on animal brain samples from various mouse models of multiple sclerosis and Alzheimer’s disease. The first test of the tractography analysis method was to determine if the tracts within the corpus collosum in the brain of mice differ between mouse models. Tracts in the corpus callosum were measured using the developed tractography analysis method. Single factor ANOVA found no differences between the tractography parameters in tracts of the corpora callosa in a mouse model of multiple sclerosis (MS) and the corresponding wildtype mouse, nor between a mouse model of Alzheimer’s disease (AD) and its corresponding wildtype mouse. The tractography analysis method was successfully developed and is now ready for use in more complex models.

scholarly journals CSF total tau, plasma and CSF p tau 181 associated with structural changes in the early stage of Alzheimer's disease

2020 ◽  
Author(s):  
Fardin Nabizadeh ◽  
Mohammad Reza Rostami ◽  
mohammad Balabandian ◽  
Niloufar Ahmadi
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Structural Changes ◽  
Clinical Symptoms ◽  
Early Stage ◽  
Cross Sectional ◽  
Total Tau ◽  
Preclinical Ad ◽  
The Brain

Abstract Alzheimer's disease (AD) is the most important cause of dementia and is a serious concern for individuals and governments worldwide. Changes in the brain appear about 15 years before the first clinical symptoms; with this in mind, it can clear the role of biomarkers in monitoring Alzheimer's development. P tau 181 level in plasma recently emerged as a new biomarker and rises obviously in AD patients, preclinical AD, and MCI patients. The role of gray matter atrophy and white matter damages in cognitive decline is well established, which is detectable by magnetic resonance imaging (MRI). In this investigation, we measured the association between CSF (total tau, and p tau 181) and plasma p tau 181 with structural changes (cortical thickness, cortical volume, surface area, and subcortical volume) in MCI patients. We performed a cross-sectional study on the ADNI cohort between 461 MCI patients. Results of voxel-wise partial correlation analysis in our participants showed a significant correlation between plasma p tau 181, CSF total tau and p tau 181 with changes in structural values in different regions. Our study revealed a significant correlation between plasma p tau and structural changes in the brain regions associated with Alzheimer's disease physiopathology. These results provide evidence for using plasma p tau 181 as a diagnostic factor in the early onset of AD patients and neurodegeneration.

scholarly journals Applying fluid biomarkers to Alzheimer's disease

2017 ◽  
Vol 313 (1) ◽  
pp. C3-C10 ◽  
Author(s):  
Henrik Zetterberg
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Medial Temporal Lobe ◽  
Clinical Symptoms ◽  
Senile Plaque ◽  
Neurofibrillary Tangle ◽  
Amyloid Β ◽  
Differential Diagnoses ◽  
Blood Tests ◽  
The Brain

Alzheimer’s disease (AD) is a common neurodegenerative disease that starts with a clinically silent phase of a decade or more during which brain pathologies accumulate predominantly in the medial temporal lobe but also elsewhere in the brain. Network dysfunction and clinical symptoms typically appear when senile plaque (amyloid-β) and neurofibrillary tangle (tau) pathologies meet in the brain parenchyma, producing synapse and neuronal loss. For plaque and tangle pathologies, reliable fluid biomarkers have been developed. These require sampling of cerebrospinal fluid. Reliable blood tests for plaque and tangle pathologies are currently lacking, but blood tests for general neurodegeneration have recently been developed. In AD, plaques and tangles often coexist with other pathologies, including Lewy bodies, and to what extent these contribute to symptoms is currently unknown. There are also important differential diagnoses that may be possible to distinguish from AD with the aid of biomarkers. The scope of this review is fluid biomarkers for AD and related pathologies. The purpose is to provide the reader with an updated account of currently available fluid biomarkers for AD and clinically relevant differential diagnoses.

Longitudinal Changes in Individual BrainAGE in Healthy Aging, Mild Cognitive Impairment, and Alzheimer’s Disease

GeroPsych ◽  
2012 ◽  
Vol 25 (4) ◽  
pp. 235-245 ◽  
Author(s):  
Katja Franke ◽  
Christian Gaser
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Healthy Aging ◽  
Brain Aging ◽  
Elderly Subjects ◽  
Additional Increase ◽  
Longitudinal Changes ◽  
Novel Method ◽  
The Brain

We recently proposed a novel method that aggregates the multidimensional aging pattern across the brain to a single value. This method proved to provide stable and reliable estimates of brain aging – even across different scanners. While investigating longitudinal changes in BrainAGE in about 400 elderly subjects, we discovered that patients with Alzheimer’s disease and subjects who had converted to AD within 3 years showed accelerated brain atrophy by +6 years at baseline. An additional increase in BrainAGE accumulated to a score of about +9 years during follow-up. Accelerated brain aging was related to prospective cognitive decline and disease severity. In conclusion, the BrainAGE framework indicates discrepancies in brain aging and could thus serve as an indicator for cognitive functioning in the future.

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