An Argument for Simple Tests of Treatment of Alzheimer’s Disease

2022 ◽  
pp. 1-4
Author(s):  
Timothy Daly ◽  
Ignacio Mastroleo ◽  
Vincent Henry ◽  
Mathieu Bourdenx
Keyword(s):  
Public Health ◽  
Risk Factors ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Public Health Policy ◽  
Lifestyle Interventions ◽  
Disease Modifying ◽  
Clinically Meaningful Outcomes ◽  
Available Information ◽  
The Web

Two potential disease-modifying approaches for dementia are being vigorously tested: the early targeting of the neuropathology of Alzheimer’s disease (AD) and multi-domain lifestyle interventions to promote resilience to neuropathology. We apply the “web of information” model of clinical translation to both approaches to argue firstly that tests of treatments aiming to achieve clinically meaningful outcomes should remain simple, and secondly, that building clinically-meaningful treatments should be kept separate from public health policy which means promoting wide-reaching action against risk factors now with available information.

Alzheimer’s disease

2020 ◽  
pp. 443-478
Author(s):  
John-Paul Taylor ◽  
Benjamin R Underwood
Keyword(s):  
Risk Factors ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cause Of Death ◽  
Clinical Features ◽  
Therapeutic Approaches ◽  
Common Cause ◽  
Disease Modifying Drugs ◽  
Future Potential ◽  
Disease Modifying

Dementia is the fifth leading cause of death worldwide. The most common cause of dementia is Alzheimer’s disease (AD). 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 AD. Importantly, the chapter explores newer evidence that has changed the way AD is viewed as regards methods of assessment using various scales to determine diagnosis, as well as current and investigative methods of treating AD. Finally, it looks at the states of disease progression, potential disease-modifying drugs for Alzheimer’s disease, and possible therapeutic approaches to treatment and management.

scholarly journals Causes and Patterns of Dementia: An Update in the Era of Redefining Alzheimer's Disease

2019 ◽  
Vol 40 (1) ◽  
pp. 65-84 ◽  
Author(s):  
Bryan D. James ◽  
David A. Bennett
Keyword(s):  
Risk Factors ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Biological Process ◽  
Brain Pathology ◽  
Dementia Risk ◽  
Dementia Syndrome ◽  
Changing Patterns ◽  
Disease Modifying ◽  
Made In

The burden of dementia continues to increase as the population ages, with no disease-modifying treatments available. However, dementia risk appears to be decreasing, and progress has been made in understanding its multifactorial etiology. The 2018 National Institute on Aging–Alzheimer's Association (NIA-AA) research framework for Alzheimer's disease (AD) defines AD as a biological process measured by brain pathology or biomarkers, spanning the cognitive spectrum from normality to dementia. This framework facilitates interventions in the asymptomatic space and accommodates knowledge that many additional pathologies (e.g., cerebrovascular) contribute to the Alzheimer's dementia syndrome. The framework has implications for how we think about risk factors for “AD”: Many commonly accepted risk factors are not related to AD pathology and would no longer be considered risk factors for AD. They may instead be related to other pathologies or resilience to pathology. This review updates what is known about causes, risk factors, and changing patterns of dementia, addressing whether they are related to AD pathology/biomarkers, other pathologies, or resilience.

P2-301: THE ALZRISK PROJECT: THE WEB-BASED CATALOGUE AND META-ANALYSIS OF FINDINGS FROM EPIDEMIOLOGIC STUDIES OF NON-GENETIC RISK FACTORS FOR ALZHEIMER'S DISEASE

2014 ◽  
Vol 10 ◽  
pp. P588-P588
Author(s):  
Bryan David James ◽  
Jennifer Weuve ◽  
Sunali Goonesekera ◽  
Meredith H. Arasaratnam ◽  
John W. Jackson ◽  
...  
Keyword(s):  
Risk Factors ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Genetic Risk ◽  
Meta Analysis ◽  
Genetic Risk Factors ◽  
Epidemiologic Studies ◽  
Web Based ◽  
The Web

scholarly journals Secondary Prevention of Dementia: Combining Risk Factors and Scalable Screening Technology

2021 ◽  
Vol 12 ◽  
Author(s):  
Triin Ojakäär ◽  
Ivan Koychev
Keyword(s):  
Risk Factors ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
At Risk ◽  
Cardiovascular Risk ◽  
Secondary Prevention ◽  
Cardiovascular Risk Factors ◽  
Digital Technologies ◽  
Increased Risk ◽  
Disease Modifying

Alzheimer's disease (AD) is a progressive neurodegenerative disorder that is the most common cause of dementia. Over a third of dementia cases are estimated to be due to potentially modifiable risk factors, thus offering opportunities for both identification of those most likely to be in early disease as well as secondary prevention. Diabetes, hypertension and chronic kidney failure have all been linked to increased risk for AD and dementia and through their high prevalence are particularly apt targets for initiatives to reduce burden of AD. This can take place through targeted interventions of cardiovascular risk factors (shown to improve cognitive outcomes) or novel disease modifying treatments in people with confirmed AD pathology. The success of this approach to secondary prevention depends on the availability of inexpensive and scalable methods for detecting preclinical and prodromal dementia states. Developments in blood-based biomarkers for Alzheimer's disease are rapidly becoming a viable such method for monitoring large at-risk groups. In addition, digital technologies for remote monitoring of cognitive and behavioral changes can add clinically relevant data to further improve personalisation of prevention strategies. This review sets the scene for this approach to secondary care of dementia through a review of the evidence for cardiovascular risk factors (diabetes, hypertension and chronic kidney disease) as major risk factors for AD. We then summarize the developments in blood-based and cognitive biomarkers that allow the detection of pathological states at the earliest possible stage. We propose that at-risk cohorts should be created based on the interaction between cardiovascular and constitutional risk factors. These cohorts can then be monitored effectively using a combination of blood-based biomarkers and digital technologies. We argue that this strategy allows for both risk factor reduction-based prevention programmes as well as for optimisation of any benefits offered by current and future disease modifying treatment through rapid identification of individuals most likely to benefit from them.

scholarly journals MULTIDOMAIN INTERVENTIONS TO PREVENT COGNITIVE IMPAIRMENT, ALZHEIMER’S DISEASE, AND DEMENTIA: FROM FINGER TO WORLD-WIDE FINGERS

2019 ◽  
pp. 1-8
Author(s):  
A. Rosenberg ◽  
F. Mangialasche ◽  
T. Ngandu ◽  
A. Solomon ◽  
M. Kivipelto
Keyword(s):  
Public Health ◽  
Risk Factors ◽  
Alzheimer’S Disease ◽  
Older Adults ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
World Wide ◽  
Clinical Decision Making ◽  
Late Onset ◽  
Increased Risk

Alzheimer’s disease (AD) and dementia are a global public health priority, and prevention has been highlighted as a pivotal component in managing the dementia epidemic. Modifiable risk factors of dementia and AD include lifestyle-related factors, vascular and metabolic disorders, and psychosocial factors. Randomized controlled clinical trials (RCTs) are needed to clarify whether modifying such factors can prevent or postpone cognitive impairment and dementia in older adults. Given the complex, multifactorial, and heterogeneous nature of late-onset AD and dementia, interventions targeting several risk factors and mechanisms simultaneously may be required for optimal preventive effects. The Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability (FINGER) is the first large, long-term RCT to demonstrate that a multidomain lifestyle-based intervention ameliorating vascular and lifestyle-related risk factors can preserve cognitive functioning and reduce the risk of cognitive decline among older adults at increased risk of dementia. To investigate the multidomain intervention in other populations and diverse cultural and geographical settings, the World-Wide FINGERS (WW-FINGERS) network was recently launched (https://alz.org/wwfingers). Within this network, new FINGER-type trials with shared core methodology, but local culture and context-specific adaptations, will be conducted in several countries. The WW-FINGERS initiative facilitates international collaborations, provides a platform for testing multidomain strategies to prevent cognitive impairment and dementia, and aims at generating high-quality scientific evidence to support public health and clinical decision-making. Furthermore, the WW-FINGERS network can support the implementation of preventive strategies and translation of research findings into practice.

scholarly journals Vascular dementia: A diagnosis running out of time

2002 ◽  
Vol 180 (2) ◽  
pp. 152-156 ◽  
Author(s):  
Robert Stewart
Keyword(s):  
Public Health ◽  
Risk Factors ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Vascular Dementia ◽  
Diagnostic Category ◽  
Vascular Risk ◽  
Public Health Measure ◽  
Health Measure ◽  
Powerful Means

BackgroundThe concept of vascular dementia has a long history but its usefulness as a diagnostic category has been called into question.AimsTo evaluate vascular disease as a risk factor for dementia and the interface between cerebrovascular pathology and Alzheimer's disease.MethodThe literature on this topic was selectively reviewed and synthesised.ResultsRisk factors for cerebrovascular disease are also risk factors for dementia. However, the course of dementia, once it has developed, appears to be frequently determined by Alzheimer's disease.ConclusionsAs a public health measure, modification of vascular risk represents a potentially powerful means to prevent dementia through delaying its onset. However, an effect on progression of dementia, once it has developed, has yet to be established. The traditional view of vascular dementia and Alzheimer's disease as distinguishable conditions is becoming steadily less tenable.

Elucidating the risk factors for progression from amyloid-negative amnestic mild cognitive impairment to dementia

2020 ◽  
Vol 17 ◽  
Author(s):  
Hyung-Ji Kim ◽  
Jae-Hong Lee ◽  
E-nae Cheong ◽  
Sung-Eun Chung ◽  
Sungyang Jo ◽  
...  
Keyword(s):  
Risk Factors ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Amnestic Mild Cognitive Impairment ◽  
Amyloid Pet ◽  
Clinical Progression ◽  
Amnestic Mci

Background: Amyloid PET allows for the assessment of amyloid β status in the brain, distinguishing true Alzheimer’s disease from Alzheimer’s disease-mimicking conditions. Around 15–20% of patients with clinically probable Alzheimer’s disease have been found to have no significant Alzheimer’s pathology on amyloid PET. However, a limited number of studies had been conducted this subpopulation in terms of clinical progression. Objective: We investigated the risk factors that could affect the progression to dementia in patients with amyloid-negative amnestic mild cognitive impairment (MCI). Methods: This study was a single-institutional, retrospective cohort study of patients over the age of 50 with amyloidnegative amnestic MCI who visited the memory clinic of Asan Medical Center with a follow-up period of more than 36 months. All participants underwent brain magnetic resonance imaging (MRI), detailed neuropsychological testing, and fluorine-18[F18]-florbetaben amyloid PET. Results: During the follow-up period, 39 of 107 patients progressed to dementia from amnestic MCI. In comparison with the stationary group, the progressed group had a more severe impairment in verbal and visual episodic memory function and hippocampal atrophy, which showed an Alzheimer’s disease-like pattern despite the lack of evidence for significant Alzheimer’s disease pathology. Voxel-based morphometric MRI analysis revealed that the progressed group had a reduced gray matter volume in the bilateral cerebellar cortices, right temporal cortex, and bilateral insular cortices. Conclusion: Considering the lack of evidence of amyloid pathology, clinical progression of these subpopulation may be caused by other neuropathologies such as TDP-43, abnormal tau or alpha synuclein that lead to neurodegeneration independent of amyloid-driven pathway. Further prospective studies incorporating biomarkers of Alzheimer’s diseasemimicking dementia are warranted.

Neuropeptides in Alzheimer’s Disease: An Update

2019 ◽  
Vol 16 (6) ◽  
pp. 544-558 ◽  
Author(s):  
Carla Petrella ◽  
Maria Grazia Di Certo ◽  
Christian Barbato ◽  
Francesca Gabanella ◽  
Massimo Ralli ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Animal Models ◽  
Potential Role ◽  
Brain Distribution ◽  
Brain Areas ◽  
Small Proteins ◽  
Current Review ◽  
The Central Nervous System ◽  
Available Information

Neuropeptides are small proteins broadly expressed throughout the central nervous system, which act as neurotransmitters, neuromodulators and neuroregulators. Growing evidence has demonstrated the involvement of many neuropeptides in both neurophysiological functions and neuropathological conditions, among which is Alzheimer’s disease (AD). The role exerted by neuropeptides in AD is endorsed by the evidence that they are mainly neuroprotective and widely distributed in brain areas responsible for learning and memory processes. Confirming this point, it has been demonstrated that numerous neuropeptide-containing neurons are pathologically altered in brain areas of both AD patients and AD animal models. Furthermore, the levels of various neuropeptides have been found altered in both Cerebrospinal Fluid (CSF) and blood of AD patients, getting insights into their potential role in the pathophysiology of AD and offering the possibility to identify novel additional biomarkers for this pathology. We summarized the available information about brain distribution, neuroprotective and cognitive functions of some neuropeptides involved in AD. The main focus of the current review was directed towards the description of clinical data reporting alterations in neuropeptides content in both AD patients and AD pre-clinical animal models. In particular, we explored the involvement in the AD of Thyrotropin-Releasing Hormone (TRH), Cocaine- and Amphetamine-Regulated Transcript (CART), Cholecystokinin (CCK), bradykinin and chromogranin/secretogranin family, discussing their potential role as a biomarker or therapeutic target, leaving the dissertation of other neuropeptides to previous reviews.

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