Appearance
Alzheimer's disease.
Literature Information
| DOI | 10.1038/nrdp.2015.56 |
|---|---|
| PMID | 27188934 |
| Journal | Nature reviews. Disease primers |
| Impact Factor | 60.6 |
| JCR Quartile | Q1 |
| Publication Year | 2015 |
| Times Cited | 837 |
| Keywords | Alzheimer's disease, amyloid-β peptide, genetic risk factors, clinical stages, biomarkers |
| Literature Type | Journal Article, Review |
| ISSN | 2056-676X |
| Pages | 15056 |
| Issue | 1() |
| Authors | Colin L Masters, Randall Bateman, Kaj Blennow, Christopher C Rowe, Reisa A Sperling, Jeffrey L Cummings |
TL;DR
Alzheimer's disease, prevalent in 10-30% of individuals over 65, has a long preclinical phase and primarily affects the elderly with sporadic forms linked to amyloid-β clearance failure. While genetic risk factors and early detection through biomarkers are advancing, current treatments mainly alleviate symptoms without addressing the disease's underlying mechanisms, highlighting the need for better management strategies that support patients and their social networks.
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Alzheimer's disease · amyloid-β peptide · genetic risk factors · clinical stages · biomarkers
Abstract
Alzheimer's disease is a chronic illness with long preclinical and prodromal phases (20 years) and an average clinical duration of 8-10 years. The disease has an estimated prevalence of 10-30% in the population >65 years of age with an incidence of 1-3%. Most patients with Alzheimer's disease (>95%) have the sporadic form, which is characterized by a late onset (80-90 years of age), and is the consequence of the failure to clear the amyloid-β (Aβ) peptide from the interstices of the brain. A large number of genetic risk factors for sporadic disease have been identified. A small proportion of patients (<1%) have inherited mutations in genes that affect processing of Aβ and develop the disease at a much younger age (mean age of ∼45 years). Detection of the accumulation of Aβ is now possible in preclinical and prodromal phases using cerebrospinal fluid biomarkers and PET. Several approved drugs ameliorate some of the symptoms of Alzheimer's disease, but no current interventions can modify the underlying disease mechanisms. Management is focused on the support of the social networks surrounding the patient and the treatment of any co-morbid illnesses, such as cerebrovascular disease.
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Primary Questions Addressed
- What are the latest findings on the interaction between lifestyle factors and Alzheimer's disease progression?
- How do emerging biomarkers like amyloid β oligomers and synaptic markers compare to traditional biomarkers in terms of diagnostic accuracy?
- What role does tau PET imaging play in the early diagnosis and differentiation of Alzheimer's disease from other types of dementia?
- How might the concept of preclinical Alzheimer's disease change the approach to early intervention and treatment strategies?
- What are the implications of combining anti-Alzheimer's therapies with lifestyle interventions for long-term patient outcomes?
Key Findings
Key Insights
Research Background and Objective: Alzheimer's disease (AD) is recognized as a chronic neurodegenerative disorder, primarily affecting the elderly population. The disease is characterized by a prolonged preclinical phase that can last up to 20 years, followed by a clinical duration of approximately 8-10 years. The aim of this research is to better understand the epidemiology, genetic factors, and pathophysiology of AD, particularly the sporadic form, which constitutes over 95% of cases. This knowledge is crucial for early detection, intervention, and ultimately improving patient outcomes.
Main Methods and Findings: The study highlights the prevalence and incidence of AD among individuals aged over 65, noting a prevalence range of 10-30% and an incidence rate of 1-3%. It identifies that the majority of cases are sporadic, occurring predominantly in individuals aged 80-90 years, and are linked to the impaired clearance of amyloid-β (Aβ) peptides in the brain. Genetic risk factors for sporadic AD have been extensively studied, while hereditary cases, accounting for less than 1%, arise from mutations affecting Aβ processing, typically manifesting at a much younger age. Advances in diagnostic methods allow for the detection of Aβ accumulation during preclinical and prodromal stages through cerebrospinal fluid biomarkers and positron emission tomography (PET) imaging. The findings also discuss the limited efficacy of approved pharmacological treatments, which primarily address symptomatic relief rather than modifying the disease's underlying mechanisms.
Core Conclusions: The research underscores that while significant strides have been made in understanding the genetic and biochemical underpinnings of Alzheimer's disease, current therapeutic options are inadequate in altering the disease's trajectory. Instead, management strategies focus on enhancing the quality of life for patients through social support and addressing co-morbid conditions, such as cerebrovascular disease.
Research Significance and Impact: This study provides critical insights into the epidemiology and biology of Alzheimer's disease, emphasizing the need for continued research into both preventive measures and innovative treatments that target the underlying disease mechanisms. The identification of genetic predispositions and advancements in early diagnostic techniques represent significant steps towards timely intervention, potentially altering the course of the disease. The findings also highlight the importance of a holistic approach in managing AD, advocating for the integration of social support systems and comprehensive care strategies to improve patient outcomes and assist caregivers. This research contributes to the broader understanding of AD, paving the way for future studies aimed at developing disease-modifying therapies and enhancing patient care frameworks.
Literatures Citing This Work
- Vascular and Metabolic Factors in Alzheimer's Disease and Related Dementias: Introduction. - Costantino Iadecola - Cellular and molecular neurobiology (2016)
- Age, APOE and sex: Triad of risk of Alzheimer's disease. - Brandalyn C Riedel;Paul M Thompson;Roberta Diaz Brinton - The Journal of steroid biochemistry and molecular biology (2016)
- The Enemy within: Innate Surveillance-Mediated Cell Death, the Common Mechanism of Neurodegenerative Disease. - Robert I Richards;Sarah A Robertson;Louise V O'Keefe;Dani Fornarino;Andrew Scott;Michael Lardelli;Bernhard T Baune - Frontiers in neuroscience (2016)
- Impairments of neural circuit function in Alzheimer's disease. - Marc Aurel Busche;Arthur Konnerth - Philosophical transactions of the Royal Society of London. Series B, Biological sciences (2016)
- High fat diet exacerbates Alzheimer's disease-related pathology in APPswe/PS1 mice. - Peter Thériault;Ayman ElAli;Serge Rivest - Oncotarget (2016)
- Hearing impairment and risk of Alzheimer's disease: a meta-analysis of prospective cohort studies. - Yuqiu Zheng;Shengnuo Fan;Wang Liao;Wenli Fang;Songhua Xiao;Jun Liu - Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology (2017)
- Unspecific binding of cRNA probe to plaques in two mouse models for Alzheimer's disease. - Anne Schaarschuch;Christoph Redies;Nicole Hertel; - Journal of negative results in biomedicine (2016)
- Close Correlation of Monoamine Oxidase Activity with Progress of Alzheimer's Disease in Mice, Observed by in Vivo Two-Photon Imaging. - Dokyoung Kim;Sung Hoon Baik;Seokjo Kang;Seo Won Cho;Juryang Bae;Moon-Yong Cha;Michael J Sailor;Inhee Mook-Jung;Kyo Han Ahn - ACS central science (2016)
- Targeting β-amyloid plaques and oligomers: development of near-IR fluorescence imaging probes. - Hongwu Liu;Jian Yang;Letian Wang;Yungen Xu;Siyuan Zhang;Jie Lv;Chongzhao Ran;Yuyan Li - Future medicinal chemistry (2017)
- Amyloid plaques beyond Aβ: a survey of the diverse modulators of amyloid aggregation. - Katie L Stewart;Sheena E Radford - Biophysical reviews (2017)
... (827 more literatures)
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