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Aging Jan 2019
Topics: Alzheimer Disease; Basal Forebrain; Cell Cycle; Humans; Septal Nuclei
PubMed: 30668543
DOI: 10.18632/aging.101777 -
Current Alzheimer Research 2018In the nineties, numerous studies began to highlight the problem of the increasing number of people with Alzheimer's disease in developed countries, especially in the... (Review)
Review
In the nineties, numerous studies began to highlight the problem of the increasing number of people with Alzheimer's disease in developed countries, especially in the context of demographic progress. At the same time, the 21st century is typical of the development of advanced technologies that penetrate all areas of human life. Digital devices, sensors, and intelligent applications are tools that can help seniors and allow better communication and control of their caregivers. The aim of the paper is to provide an up-to-date summary of the use of technological solutions for improving health and safety for people with Alzheimer's disease. Firstly, the problems and needs of senior citizens with Alzheimer's disease (AD) and their caregivers are specified. Secondly, a scoping review is performed regarding the technological solutions suggested to assist this specific group of patients. Works obtained from the following libraries are used in this scoping review: Web of Science, PubMed, Springer, ACM and IEEE Xplore. Four independent reviewers screened the identified records and selected relevant articles which were published in the period from 2007 to 2018. A total of 6,705 publications were selected. In all, 128 full papers were screened. Results obtained from the relevant studies were furthermore divided into the following categories according to the type and use of technologies: devices, processing, and activity recognition. The leading technological solution in the category of devices are wearables and ambient noninvasive sensors. The introduction and utilization of these technologies, however, bring about challenges in acceptability, durability, ease of use, communication, and power requirements. Furthermore, it needs to be pointed out that these technological solutions should be based on open standards.
Topics: Aging; Alzheimer Disease; Computer-Assisted Instruction; Humans; Wearable Electronic Devices
PubMed: 29701154
DOI: 10.2174/1567205015666180427124547 -
Journal of Alzheimer's Disease : JAD 2018The amyloid-β oligomer (AβO) hypothesis was introduced in 1998. It proposed that the brain damage leading to Alzheimer's disease (AD) was instigated by soluble,... (Review)
Review
The amyloid-β oligomer (AβO) hypothesis was introduced in 1998. It proposed that the brain damage leading to Alzheimer's disease (AD) was instigated by soluble, ligand-like AβOs. This hypothesis was based on the discovery that fibril-free synthetic preparations of AβOs were potent CNS neurotoxins that rapidly inhibited long-term potentiation and, with time, caused selective nerve cell death (Lambert et al., 1998). The mechanism was attributed to disrupted signaling involving the tyrosine-protein kinase Fyn, mediated by an unknown toxin receptor. Over 4,000 articles concerning AβOs have been published since then, including more than 400 reviews. AβOs have been shown to accumulate in an AD-dependent manner in human and animal model brain tissue and, experimentally, to impair learning and memory and instigate major facets of AD neuropathology, including tau pathology, synapse deterioration and loss, inflammation, and oxidative damage. As reviewed by Hayden and Teplow in 2013, the AβO hypothesis "has all but supplanted the amyloid cascade." Despite the emerging understanding of the role played by AβOs in AD pathogenesis, AβOs have not yet received the clinical attention given to amyloid plaques, which have been at the core of major attempts at therapeutics and diagnostics but are no longer regarded as the most pathogenic form of Aβ. However, if the momentum of AβO research continues, particularly efforts to elucidate key aspects of structure, a clear path to a successful disease modifying therapy can be envisioned. Ensuring that lessons learned from recent, late-stage clinical failures are applied appropriately throughout therapeutic development will further enable the likelihood of a successful therapy in the near-term.
Topics: Alzheimer Disease; Amyloid beta-Peptides; Animals; Humans; Models, Neurological
PubMed: 29843241
DOI: 10.3233/JAD-179941 -
European Journal of Nuclear Medicine... Dec 2019Neuroinflammation, as defined by the activation of microglia and astrocytes, has emerged in the last years as a key element of the pathogenesis of neurodegenerative... (Review)
Review
Neuroinflammation, as defined by the activation of microglia and astrocytes, has emerged in the last years as a key element of the pathogenesis of neurodegenerative diseases based on genetic findings and preclinical and human studies. This has raised the need for new methodologies to assess and follow glial activation in patients, prompting the development of PET ligands for molecular imaging of glial cells and novel structural MRI and DTI tools leading to a multimodal approach. The present review describes the recent advancements in microglia and astrocyte biology in the context of health, ageing, and Alzheimer's disease, the most common dementia worldwide. The review further delves in molecular imaging discussing the challenges associated with past and present targets, including conflicting findings, and finally, presenting novel methodologies currently explored to improve our in vivo knowledge of the neuroinflammatory patterns in Alzheimer's disease. With glial cell activation as a potential therapeutic target in neurodegenerative diseases, the translational research between cell biologists, chemists, physicists, radiologists, and neurologists should be strengthened.
Topics: Alzheimer Disease; Astrocytes; Cognitive Dysfunction; Humans; Inflammation; Neuroimaging; Receptors, GABA
PubMed: 31396666
DOI: 10.1007/s00259-019-04462-w -
BioMed Research International 2021Alzheimer's disease is a neurodegenerative disorder that is caused by the accumulation of beta-amyloid plaques in the brain. Currently, there is no definitive cure... (Review)
Review
Alzheimer's disease is a neurodegenerative disorder that is caused by the accumulation of beta-amyloid plaques in the brain. Currently, there is no definitive cure available to treat Alzheimer's disease. The available medication in the market has the ability to only slow down its progression. However, nanotechnology has shown its superiority that can be applied for medical usage and it has a great potential in the therapy of Alzheimer's disease, specifically in the disease diagnosis and providing an alternative approach to treat Alzheimer's disease. This is done by increasing the efficiency of drug delivery by penetrating and overcoming the blood-brain barrier. Having said that, there are limitations that need to be further investigated and researched in order to minimize the adverse effects and potential toxicity and to improve drug bioavailability. The recent advances in the treatment of Alzheimer's disease using nanotechnology include the regeneration of stem cells, nanomedicine, and neuroprotection. In this review, we will discuss the advancement of nanotechnology which helps in the diagnosis and treatment of neurodegenerative disorders such as Alzheimer's disease as well as its challenges.
Topics: Alzheimer Disease; Animals; Drug Delivery Systems; Genetic Therapy; Humans; Immunotherapy; Nanoparticles; Nanotechnology
PubMed: 34285915
DOI: 10.1155/2021/5550938 -
Journal of Alzheimer's Disease : JAD 2018In the last decades, progress in neuroimaging techniques and cerebrospinal fluid assays has enabled the characterization of several Alzheimer's disease (AD) biomarkers.... (Review)
Review
In the last decades, progress in neuroimaging techniques and cerebrospinal fluid assays has enabled the characterization of several Alzheimer's disease (AD) biomarkers. This knowledge has shifted the conceptualization of AD from a clinical-pathological construct, where its diagnosis required the presence of dementia with distinct pathologic features, toward a clinical-biological one that recognizes AD as a pathological continuum with a clinical picture that ranges from normal cognition to a dementia stage. Specifically, AD is now divided into three stages: preclinical (abnormal biomarkers and no or only subtle cognitive impairment), mild cognitive impairment or prodromal AD (abnormal pathophysiological biomarkers and episodic memory impairment), and dementia (abnormal biomarkers and clear cognitive and functional impairment). The possibility of assessing AD pathophysiology in vivo before the onset of clinical symptoms in the preclinical stage provides the unprecedented opportunity to intervene at earlier stages of the continuum in secondary prevention trials. Currently, large cohort studies of cognitively healthy participants are undergoing with the main aim of disentangling the natural history of AD to identify individuals with an increased risk of developing AD in the near future to be recruited in these clinical trials. In this paper, we review how the concept of AD has changed over the years as well as discuss the implications of this conceptual change.
Topics: Alzheimer Disease; Biomarkers; Disease Progression; Humans; Models, Biological
PubMed: 29562531
DOI: 10.3233/JAD-170698 -
Folia Neuropathologica 2012In this paper we review the hard-earned data, which present ischemic induction of amyloid precursor protein, presenilins, apolipoproteins and secretases genes, playing... (Review)
Review
In this paper we review the hard-earned data, which present ischemic induction of amyloid precursor protein, presenilins, apolipoproteins and secretases genes, playing key roles in β-amyloid peptide generation. Presented data are strongly supporting a hypothesis that brain ischemia may be involved in the aetiology of sporadic Alzheimer's disease. Potential contribution and impact of ischemically activated genes on the development of sporadic Alzheimer's disease remain to be established at both genetic and functional levels. The identification of the genes involved in sporadic Alzheimer's disease induced by ischemia will enable to further define the events leading to Alzheimer's disease-related abnormalities. Additionally, knowledge gained from the reviewed studies should facilitate the elaboration of effective treatment and/or prevention of sporadic Alzheimer's disease.
Topics: Alzheimer Disease; Animals; Brain Ischemia; Humans
PubMed: 23319188
DOI: 10.5114/fn.2012.32362 -
Journal of Lipid Research Oct 2017Alzheimer's disease (AD) is characterized by an extensive accumulation of amyloid-β (Aβ) peptide, which triggers a set of deleterious processes, including synaptic... (Review)
Review
Alzheimer's disease (AD) is characterized by an extensive accumulation of amyloid-β (Aβ) peptide, which triggers a set of deleterious processes, including synaptic dysfunction, inflammation, and neuronal injury, leading to neuronal loss and cognitive impairment. A large body of evidence supports that nuclear receptor (NR) activation could be a promising therapeutic approach for AD. NRs are ligand-activated transcription factors that regulate gene expression and have cell type-specific effects. In this review, we discuss the mechanisms that underlie the beneficial effects of NRs in AD. Moreover, we summarize studies reported in the last 10-15 years and their major outcomes arising from the pharmacological targeting of NRs in AD animal models. The dissection of the pathways regulated by NRs in the context of AD is of importance in identifying novel and effective therapeutic strategies.
Topics: Alzheimer Disease; Animals; Humans; Receptors, Cytoplasmic and Nuclear
PubMed: 28264880
DOI: 10.1194/jlr.R075556 -
Aging Oct 2018
Topics: Alzheimer Disease; Animals; Brain; Cognition; Drug Design; Humans; Memory; Nootropic Agents; Risk Factors; Risk Reduction Behavior
PubMed: 30317224
DOI: 10.18632/aging.101581 -
Revista Medica de Chile Apr 2017Type 2 diabetes and obesity are possible risk factors for Alzheimers disease and these can be modified by physical activity and changes in dietary patterns, such as... (Review)
Review
Type 2 diabetes and obesity are possible risk factors for Alzheimers disease and these can be modified by physical activity and changes in dietary patterns, such as switching to a Mediterranean diet. This diet includes fruits, vegetables, olive oil, fish and moderate wine intake. These foods provide vitamins, polyphenols and unsaturated fatty acids. This diet should be able to reduce oxidative stress. The inflammatory response is also reduced by unsaturated fatty acids, resulting in a lower expression and a lower production of pro-inflammatory cytokines. The Cardiovascular protection is related to the actions of polyphenols and unsaturated fatty acids on the vascular endothelium. The Mediterranean diet also can improve cardiovascular risk factors such as dyslipidemia, hypertension and metabolic syndrome. These beneficial effects of the Mediterranean diet should have a role in Alzheimers disease prevention.
Topics: Alzheimer Disease; Diet, Mediterranean; Humans; Oxidative Stress; Risk Factors
PubMed: 28748997
DOI: 10.4067/S0034-98872017000400010