Top Research Papers on Alzheimer's Disease

Recognition that chronologic age is not per se a cause of dementia opens the way for a more active approach to Alzheimer-type dementias as a specific disease syndrome.

This protocol for a Cochrane Review (Intervention) aims to clearly define the clinical efficacy and safety of Tramiprosate for the treatment of Alzheimer's disease.

Alzhemed appears to be well tolerated with long-term exposure and reduces CSF Abeta(42) levels in mild-to-moderate AD subjects, and these findings will be discussed in the context of two large-scale randomized, double-blind, placebo-controlled Phase III clinical trials that are currently being conducted to test the long- term safety and efficacy of Alzhemed.

What AD is, the main areas in which researchers are working, and new approaches for helping families and friends care for people with AD are described.

An alternative approach is proposed which insists on Alzheimer's reasoning and argues that he neither 'discovered' nor 'created', but invented AD.

Alzheimer achieved worldwide recognition when he was mentioned for the first time to name the disease of what Auguste got in the 8th edition of Handbook of Psychiatry.

Alois Alzheimer is credited with identifying the fi rst published case of “presenile dementia”, which Kraepelin would later identify as Alzheimer’s disease.

Not until 1993-94 did researchers agreed that AD had a heterogenous etiology that shared the same clinical (behavioral and cognitive) presenration, and recent research suggests that different pathogenic pathways lead to a similar pathologic endpoint.

It is argued that Alzheimer disease pathology represents a final common pattern of changes that results from several or possibly many different aetiologies, which might better guide future research into late onset dementias.

The prevalence of AD in Australia, and associated costs of caring for individuals afflicted with this disease, are projected to quadruple by 2050, and it is necessary to find modifiable factors that may alter the incidence and prevalence of this disease.

Recent advances in the neuropathologic basis of Alzheimer’s disease include the conceptualization and study of the preclinical phase of AD, mild cognitive impairment, mixed pathologies, and the specific roles of β-amyloid and hyperphosphorylated tau protein.

The authors can slow Alzheimer’s but cannot prevent or stop it till now, so some non-drug treatments, like physical activity, social engagement, nutritious supplemented food, and FDA approved drugs helps to reduce AD.

Maybe you have knowledge that, people have search hundreds of times for their favorite books like this genetics and alzheimers disease research and perspectives in alzheimer's disease, but end up in infectious downloads.

The path from establishing the Alzheimer Disease Societies Croatia to obtaining full membership of Alzheimer's Disease International federation and provisional members of Alzheimer Europe is described.

Heterogeneity of Alzheimer's disease predicts complex clinical presentations in people living with AD and may raise awareness of a healthy lifestyle as potential prevention and treatment of the comorbidities.

To compare endothelial function of people with Alzheimer's disease (AD) with that of people without, a large number of patients with and without the disease are fitted with EMTs.

The heterogeneity of Alzheimer’s disease predicts complex clinical presentations in people living with AD, and the genes define AD as a part of age-related comorbidities with shared biological mechanisms and may raise awareness of a healthy lifestyle as potential prevention and treatment of the comorbidities.

Alzheimer's disease, the commonest cause of dementia, is a growing global health concern with huge implications for individuals and society. In this review, current understanding of the epidemiology, genetics, pathology and pathogenesis of Alzheimer's disease is outlined, before its clinical presentation and current treatment strategies are discussed. Finally, the review discusses how our enhanced understanding of Alzheimer pathogenesis, including the recognition of a protracted preclinical phase, is informing new therapeutic strategies with the aim of moving from treatment to prevention.

From the Department of Neurology, Caritas St. Elizabeth’s Medical Center, Brighton, MA, this work is supported by the Warren Alpert Medical School at Brown University, Providence.

The benefits of early investigation and diagnosis of Alzheimer's disease include instigation of pharmacological symptomatic treatments and initiation of psychosocial support, plus treatment of comorbid conditions.

Pharmacologic treatment with thiazolidinedions, agonists of the nuclear receptor peroxisome proliferator-activated receptor gamma (PPARgamma), may offer some therapeutic relief of AD by lowering peripheral insulin and enhancing insulin sensitivity.

Application of diagnostic methods increases, partly due to improved awareness of cognitive symptoms and the relevance of early detection and diagnosis, in particular when more efficient disease-modifying drugs become available.

No therapy is proven to delay disease progression, but recent insights into the pathophysiology of AD have led to promising investigational therapies, including the development of both γ- and β-secretase inhibitors as well as active and passive immunization against the amyloid β-protein.

It is perhaps premature to rule out circulatory factors, especially since the authors now know about the importance of the extracranial circulation, but arteriosclerotic stenoses could cause cerebrovascular insufficiency which would explain this woman’s fluctuating and progressive symptoms.

Alzheimer disease is a relentlessly progressive degenerative disorder of the human central nervous system that typically begins in middle to late adult life and is manifested by a series of clinical features, with recent and immediate recall being affected more than remote recall.

A formula was developed to convert one test score to the other and both tests demonstrated test-retest reliability coefficients of 0.75 and above.

In postmortem cortical tissue from Alzheimer patients, somatostatin levels were lower in posterior parietal but not in anterior frontal cortex, suggesting loss of som atostatin-containing neurons, especially in the parietal association cortex, may be a critical determinant for Alzheimer dementia.

The treatment for Alzheimer’s disease at this point focuses on symptomatic relief, and attempts at finding easily applied preventative measures have not been successful.

Memory loss is the most common sign of Alzheimer disease, and the loss of memory worsens over time until it interferes with most aspects of daily living.

The clinical features of a case of Alzheimer’s disease and a histochemical and morphologic analysis of a cerebral biopsy are reported and the histochemical technics to be described are being used as a laboratory routine for extensive mappings of the normal human brain.

Throughout the limbic system and neocortex of the patient were large numbers of senile plaques and neurofibrillary tangles, the pathological hallmarks of AD.

Recent findings concerning AD pathogenesis are reviewed with a particular focus on how Ab impacts synapses, the peptide that aggregates to form senile plaques in the brain of AD patients.

This work is licensed under a Creative Commons Attribution 4.0 International License, which means that users will need to obtain permission from the license holder to reproduce the material.

Alzheimer's is evaluated by identifying certain symptoms and ruling out other possible causes of dementia, including neurological, blood and brain imaging exams, such as CT, MRI or PET/CT of the head.

It is discussed how elucidating the genotype-to-phenotype relationships of familial forms of Alzheimer's disease has highlighted the importance of the misfolding and altered proteostasis of two otherwise soluble proteins, amyloid β-protein and tau, suggesting mechanism-based therapeutic targets that have led to clinical trials.

The next generation of particle accelerators will be able to combine high-performance liquid chromatography with high-resolution 3D image analysis to provide real-time information about the response of the immune system.

The low prevalence and incidence of DSM-III-R major depression in these patients suggest that for the period of time the patients were followed up, Alzheimer’s disease did not predispose to major depression, however, major depression may herald the subsequent onset of dementia.

Overall there is still no evidence that short term treatment of enteric infections with antibiotics prevents reactive arthritis, but treatment ofchlamydial infections does probably reduce the risks of postvenereal arthritis.

The role of stress as one of the trigger factors in the aging of the hippocampus structures and its damage in Alz-heimer's disease and changes in cerebral microcirculation, the state of the blood-brain barrier and the participation of stress-related mechanisms in them as a single complex are discussed.

How neuroimaging techniques promise to characterize the brain changes which precede the onset of cognitive impairment in persons at risk for Alzheimer's disease and identify treatments to preventThe onset of dementia is considered.

Advances in understanding the pathogenetic cascade of events that characterize AD provide a framework for early detection and therapeutic interventions, including transmitter replacement therapies, antioxidants, anti-inflammatory agents, estrogens, nerve growth factor, and drugs that prevent amyloid formation in the brain.

The historical evolution of concepts of senile dementia and Alzheimer's disease are outlined and it is suggested that the evolution of conceptions of the disease have been influenced as much by notions of what constituted "normal aging" as by scientific research concerned with understanding ageassociated neurological diseases.

In their article, “Imaging markers for Alzheimer disease: Which vs how,” Dr. Frisoni and his colleagues looked carefully at the ways in which doctors evaluate Alzheimer disease and another problem with cognition called mild cognitive impairment.

Memory loss is the most common sign of Alzheimer disease, and the loss of memory worsens over time until it interferes with most aspects of daily living.

From an uncommon process, Alzheimer’s disease has now been elevated to the status of a major lethal disease and, consequently, accelerated research investigations have provided insight into its nature.

This book brings together an international team of experts to provide a comprehensive and up-to-date overview of AD, providing the readers with a broad picture of the underlying neuropathology, genetics, proteomics, risk factors, novel biomarkers, and potential interventions.

This fully updated and revised chapter comprehensively reviews the latest evidence on diagnosis, assessment, investigations, clinical features, management, risk factors, prognosis, and future potential treatments for Alzheimer’s disease.

The latest criteria for the diagnosis of AD is described, including earliest diagnostic stage of preclinical AD, which has the highest potential for research, including diagnosis and disease modification.

Pacemaker implantation may be of risk in patients with Alzheimer’s disease, especially in those aged ≥75 years, and in patients in group 2, which had 3 times higher rate of complication than those without an AD and aged ≤75 years.

Structural MRI studies have demonstrated that MTL volumes predict progression to AD from mild states of memory impairment and correlate with impaired memory performance in AD patients, supporting the contention that M TL volumetric measures are both clinically and biologically relevant.