Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Advances in Alzheimer's imaging are changing the experience of Alzheimer's disease.

ABSTRACT: Neuroimaging is advancing a new definition of Alzheimer's disease (AD). Using imaging biomarkers, clinicians may begin to diagnose the disease by identifying pathology and neurodegeneration in either cognitively impaired or unimpaired adults. This "biomarker-based" diagnosis may allow clinicians novel opportunities to use interventions that either delay the onset or slow the progression of cognitive decline, but it will also bring novel challenges. How will changing the definition of AD from a clinical to a biomarker construct change the experience of living with the disease? Knowledge of AD biomarker status can affect how individuals feel about themselves (internalized stigma) and how others judge them (public stigma). Following a review of AD stigma, we appraise how advances in diagnosis may enable or interrupt its transfer from clinical to preclinical stages and then explore conceptual and pragmatic challenges to addressing stigma in routine care.

SUBMITTER: Stites SD

PROVIDER: S-EPMC5956938 | biostudies-other | 2018

REPOSITORIES: biostudies-other

ACCESS DATA

Json Xml

Publications

Advances in Alzheimer's imaging are changing the experience of Alzheimer's disease.

Stites Shana D SD Milne Richard R Karlawish Jason J

Alzheimer's & dementia (Amsterdam, Netherlands) 20180319

Neuroimaging is advancing a new definition of Alzheimer's disease (AD). Using imaging biomarkers, clinicians may begin to diagnose the disease by identifying pathology and neurodegeneration in either cognitively impaired or unimpaired adults. This "biomarker-based" diagnosis may allow clinicians novel opportunities to use interventions that either delay the onset or slow the progression of cognitive decline, but it will also bring novel challenges. How will changing the definition of AD from a c ...[more]

PMID: 29780873

Similar Datasets

Recent advances in imaging Alzheimer's disease.

Project description:Advances in brain imaging technology in the past five years have contributed greatly to the understanding of Alzheimer's disease (AD). Here, we review recent research related to amyloid imaging, new methods for magnetic resonance imaging analyses, and statistical methods. We also review research that evaluates AD risk factors and brain imaging, in the context of AD prediction and progression. We selected a variety of illustrative studies, describing how they advanced the field and are leading AD research in promising new directions.

| S-EPMC4110110 | biostudies-literature

Recent Advances in Imaging of Preclinical, Sporadic, and Autosomal Dominant Alzheimer's Disease.

Project description:Observing Alzheimer's disease (AD) pathological changes in vivo with neuroimaging provides invaluable opportunities to understand and predict the course of disease. Neuroimaging AD biomarkers also allow for real-time tracking of disease-modifying treatment in clinical trials. With recent neuroimaging advances, along with the burgeoning availability of longitudinal neuroimaging data and big-data harmonization approaches, a more comprehensive evaluation of the disease has shed light on the topographical staging and temporal sequencing of the disease. Multimodal imaging approaches have also promoted the development of data-driven models of AD-associated pathological propagation of tau proteinopathies. Studies of autosomal dominant, early sporadic, and late sporadic courses of the disease have shed unique insights into the AD pathological cascade, particularly with regard to genetic vulnerabilities and the identification of potential drug targets. Further, neuroimaging markers of b-amyloid, tau, and neurodegeneration have provided a powerful tool for validation of novel fluid cerebrospinal and plasma markers. This review highlights some of the latest advances in the field of human neuroimaging in AD across these topics, particularly with respect to positron emission tomography and structural and functional magnetic resonance imaging.

| S-EPMC8423933 | biostudies-literature

Advances in the prevention of Alzheimer's Disease.

Project description:Alzheimer's disease (AD), the leading cause of dementia, has reached epidemic proportions, with major social, medical and economical burdens. With no currently available curative treatments, both the World Health Organization and the G8 Dementia Summit recently identified dementia and AD prevention as a major public health priority. Dementia and AD have a wide range of risk factors (genetic, vascular/metabolic and lifestyle-related), which often co-occur and thus interact with each other. Previous intervention efforts aimed at preventing dementia and AD focused on the management of single risk factors, with relatively modest findings. Also, the effect of risk factors depends on age at exposure, indicating that the timing of preventive interventions needs to be carefully considered. In view of the complex multifactorial nature of AD, as well as its long pre-clinical (asymptomatic) phase, interventions simultaneously targeting multiple risk factors and disease mechanisms at an early stage of the disease are most likely to be effective. Three large European multidomain prevention trials have been launched with the goal of preventing cognitive decline, dementia and AD in older adults with different risk profiles. Pharmacological trials are also shifting towards prevention of Alzheimer dementia, by targeting at-risk individuals prior to the onset of cognitive symptoms. The current review will summarize and discuss the evidence on risk and protective factors from observational studies, ongoing lifestyle-related and pharmacological randomized controlled trials (RCTs), as well as future directions for dementia and AD prevention.

| S-EPMC4447057 | biostudies-literature

Recent Advances: Decoding Alzheimer's Disease With Stem Cells.

Project description:Alzheimer's disease (AD) is an irreversible neurodegenerative disorder that destroys cognitive functions. Recently, a number of high-profile clinical trials based on the amyloid cascade hypothesis have encountered disappointing results. The failure of these trials indicates the necessity for novel therapeutic strategies and disease models. In this review, we will describe how recent advances in stem cell technology have shed light on a novel treatment strategy and revolutionized the mechanistic investigation of AD pathogenesis. Current advances in promoting endogenous neurogenesis and transplanting exogenous stem cells from both bench research and clinical translation perspectives will be thoroughly summarized. In addition, reprogramming technology-based disease modeling, which has shown improved efficacy in recapitulating pathological features in human patients, will be discussed.

| S-EPMC5874773 | biostudies-literature

Advances in Genetic and Molecular Understanding of Alzheimer's Disease.

Project description:Alzheimer's disease (AD) has become a common disease of the elderly for which no cure currently exists. After over 30 years of intensive research, we have gained extensive knowledge of the genetic and molecular factors involved and their interplay in disease. These findings suggest that different subgroups of AD may exist. Not only are we starting to treat autosomal dominant cases differently from sporadic cases, but we could be observing different underlying pathological mechanisms related to the amyloid cascade hypothesis, immune dysfunction, and a tau-dependent pathology. Genetic, molecular, and, more recently, multi-omic evidence support each of these scenarios, which are highly interconnected but can also point to the different subgroups of AD. The identification of the pathologic triggers and order of events in the disease processes are key to the design of treatments and therapies. Prevention and treatment of AD cannot be attempted using a single approach; different therapeutic strategies at specific disease stages may be appropriate. For successful prevention and treatment, biomarker assays must be designed so that patients can be more accurately monitored at specific points during the course of the disease and potential treatment. In addition, to advance the development of therapeutic drugs, models that better mimic the complexity of the human brain are needed; there have been several advances in this arena. Here, we review significant, recent developments in genetics, omics, and molecular studies that have contributed to the understanding of this disease. We also discuss the implications that these contributions have on medicine.

| S-EPMC8394321 | biostudies-literature

Advances in developing novel therapeutic strategies for Alzheimer's disease.

Project description:Alzheimer's Disease (AD), the most prevalent neurodegenerative disease of aging, affects one in eight older Americans. Nearly all drug treatments tested for AD today have failed to show any efficacy. There is a great need for therapies to prevent and/or slow the progression of AD. The major challenge in AD drug development is lack of clarity about the mechanisms underlying AD pathogenesis and pathophysiology. Several studies support the notion that AD is a multifactorial disease. While there is abundant evidence that amyloid plays a role in AD pathogenesis, other mechanisms have been implicated in AD such as tangle formation and spread, dysregulated protein degradation pathways, neuroinflammation, and loss of support by neurotrophic factors. Therefore, current paradigms of AD drug design have been shifted from single target approach (primarily amyloid-centric) to developing drugs targeted at multiple disease aspects, and from treating AD at later stages of disease progression to focusing on preventive strategies at early stages of disease development. Here, we summarize current strategies and new trends of AD drug development, including pre-clinical and clinical trials that target different aspects of disease (mechanism-based versus non-mechanism based, e.g. symptomatic treatments, lifestyle modifications and risk factor management).

| S-EPMC6291983 | biostudies-literature

Current Advances in Mitochondrial Targeted Interventions in Alzheimer's Disease.

Project description:Alzheimer's disease is the most prevalent neurodegenerative disorder and affects the lives not only of those who are diagnosed but also of their caregivers. Despite the enormous social, economic and political burden, AD remains a disease without an effective treatment and with several failed attempts to modify the disease course. The fact that AD clinical diagnosis is most often performed at a stage at which the underlying pathological events are in an advanced and conceivably irremediable state strongly hampers treatment attempts. This raises the awareness of the need to identify and characterize the early brain changes in AD, in order to identify possible novel therapeutic targets to circumvent AD's cascade of events. One of the most auspicious targets is mitochondria, powerful organelles found in nearly all cells of the body. A vast body of literature has shown that mitochondria from AD patients and model organisms of the disease differ from their non-AD counterparts. In view of this evidence, preserving and/or restoring mitochondria's health and function can represent the primary means to achieve advances to tackle AD. In this review, we will briefly assess and summarize the previous and latest evidence of mitochondria dysfunction in AD. A particular focus will be given to the recent updates and advances in the strategy options aimed to target faulty mitochondria in AD.

| S-EPMC10525414 | biostudies-literature

Alzheimer's disease

Project description:Alzheimer's disease

| PRJNA683625 | ENA

Changing the course of Alzheimer's disease: anti-amyloid disease-modifying treatments on the horizon.

Project description:To review the amyloid hypothesis as the predominant mechanistic theory of Alzheimer's disease and update the status of new disease-modifying, anti-amyloid treatments in clinical development.Governmental Web sites and those of professional Alzheimer's disease associations and drug manufacturers were searched for new drugs in development. An English-language search of PubMed (January 2003-January 2006) was conducted using the search terms Alzheimer's disease and amyloid hypothesis and each of the drugs and immunotherapies from the 4 identified classes of anti-amyloid, disease-modifying therapies.Studies and reports were selected on the basis of recent publication, adequate methodology, and completeness of data.Immunotherapy, ?-secretase inhibitors, selective neurotoxic aggregated 42-amino acid peptide subspecies of amyloid ? (A???)-lowering agents (tarenflurbil), inhibitors of amyloid aggregation (tramiprosate), and statins show promise in clinical trials. Safety remains an important factor. Disease-modifying drugs that specifically target the amyloid cascade and do not interact with essential biological pathways are expected to possess a lower rate of unintended adverse events.Agents that selectively target A??? production (e.g., tarenflurbil), block A? aggregation (e.g., tramiprosate), or enhance alpha-secretase activity (statins) offer hope for disease modification and prevention and do not appear to interfere with other biological pathways.Discovery of safe and effective disease-modifying therapies will usher in a new age of Alzheimer's disease treatment.

| S-EPMC1894844 | biostudies-other

Mitochondria dysfunction in the pathogenesis of Alzheimer's disease: recent advances.

Project description:Alzheimer's disease (AD) is one of the most prevalent neurodegenerative diseases, characterized by impaired cognitive function due to progressive loss of neurons in the brain. Under the microscope, neuronal accumulation of abnormal tau proteins and amyloid plaques are two pathological hallmarks in affected brain regions. Although the detailed mechanism of the pathogenesis of AD is still elusive, a large body of evidence suggests that damaged mitochondria likely play fundamental roles in the pathogenesis of AD. It is believed that a healthy pool of mitochondria not only supports neuronal activity by providing enough energy supply and other related mitochondrial functions to neurons, but also guards neurons by minimizing mitochondrial related oxidative damage. In this regard, exploration of the multitude of mitochondrial mechanisms altered in the pathogenesis of AD constitutes novel promising therapeutic targets for the disease. In this review, we will summarize recent progress that underscores the essential role of mitochondria dysfunction in the pathogenesis of AD and discuss mechanisms underlying mitochondrial dysfunction with a focus on the loss of mitochondrial structural and functional integrity in AD including mitochondrial biogenesis and dynamics, axonal transport, ER-mitochondria interaction, mitophagy and mitochondrial proteostasis.

| S-EPMC7257174 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data