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Curated Papers > High-Impact Authority Literature on "Alzheimer's Disease"

Alzheimer's disease. ​

Literature Information ​

DOI10.1016/S0140-6736(06)69113-7
PMID16876668
JournalLancet (London, England)
Publication Year2006
Times Cited1230
KeywordsAlzheimer's disease, dementia, amyloid beta, hyperphosphorylated tau, genetic factors
Literature TypeJournal Article, Review
ISSN0140-6736
Pages387-403
Issue368(9533)
AuthorsKaj Blennow, Mony J de Leon, Henrik Zetterberg

TL;DR ​

This seminar reviews the complexities of Alzheimer's disease, highlighting the distinction between rare familial forms caused by specific genetic mutations and the more common sporadic cases, which lack a clear cause due to their heterogeneous nature influenced by age and various risk factors. The findings underscore the need for a multifaceted approach to understanding the disease's molecular pathogenesis and developing effective treatments, given its significant impact on millions worldwide.

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Alzheimer's disease · dementia · amyloid beta · hyperphosphorylated tau · genetic factors

Abstract ​

Alzheimer's disease is the most common cause of dementia. Research advances have enabled detailed understanding of the molecular pathogenesis of the hallmarks of the disease--ie, plaques, composed of amyloid beta (Abeta), and tangles, composed of hyperphosphorylated tau. However, as our knowledge increases so does our appreciation for the pathogenic complexity of the disorder. Familial Alzheimer's disease is a very rare autosomal dominant disease with early onset, caused by mutations in the amyloid precursor protein and presenilin genes, both linked to Abeta metabolism. By contrast with familial disease, sporadic Alzheimer's disease is very common with more than 15 million people affected worldwide. The cause of the sporadic form of the disease is unknown, probably because the disease is heterogeneous, caused by ageing in concert with a complex interaction of both genetic and environmental risk factors. This seminar reviews the key aspects of the disease, including epidemiology, genetics, pathogenesis, diagnosis, and treatment, as well as recent developments and controversies.

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Primary Questions Addressed ​

  1. What are the latest findings on the interaction between lifestyle factors and Alzheimer's disease progression?
  2. How do emerging biomarkers like amyloid β oligomers and synaptic markers compare to traditional biomarkers in terms of diagnostic accuracy?
  3. What role does tau PET imaging play in the early diagnosis and differentiation of Alzheimer's disease from other types of dementia?
  4. How might the concept of preclinical Alzheimer's disease change the approach to early intervention and treatment strategies?
  5. What are the implications of combining anti-Alzheimer's therapies with lifestyle interventions for long-term patient outcomes?

Key Findings ​

Key Insights on Alzheimer's Disease

  1. Research Background and Purpose: Alzheimer's disease (AD) is recognized as the leading cause of dementia, significantly impacting millions globally. The primary aim of this research is to explore the molecular pathogenesis of AD, focusing on its fundamental characteristics—amyloid plaques and tau tangles. By examining both familial (early-onset) and sporadic (late-onset) forms of the disease, the study seeks to provide a comprehensive understanding of the genetic and environmental factors influencing AD, thereby improving diagnostics and treatment strategies.

  2. Main Methods and Findings: The research integrates epidemiological data, genetic analysis, and insights into the pathophysiological mechanisms underlying AD. It highlights the role of amyloid beta (Abeta) in plaque formation and hyperphosphorylated tau in tangle formation. Familial AD, though rare, is linked to specific mutations in the amyloid precursor protein and presenilin genes, confirming a direct genetic basis for the disease. In contrast, sporadic AD, which affects over 15 million individuals worldwide, is characterized by its complex etiology, involving age-related changes and a myriad of genetic and environmental interactions. This complexity complicates the identification of singular causative factors, necessitating a multi-faceted research approach.

  3. Core Conclusions: The findings underscore the dual nature of Alzheimer's disease: the rare familial form with clear genetic markers and the more prevalent sporadic form, which remains enigmatic due to its heterogeneous causes. There is a growing recognition that both genetic predisposition and environmental influences play critical roles in the disease's onset and progression. This duality highlights the necessity for tailored research and treatment approaches that consider both genetic and non-genetic factors.

  4. Research Significance and Impact: This seminar's insights hold substantial implications for public health and clinical practices. Understanding the molecular underpinnings of Alzheimer's disease paves the way for developing targeted therapies and preventative strategies. Additionally, recognizing the heterogeneity of sporadic AD emphasizes the need for personalized medicine approaches in treatment and diagnosis. The ongoing research into the disease's complexities may lead to breakthroughs that could alleviate the burden of dementia on individuals and healthcare systems worldwide, fostering a deeper understanding of cognitive decline and enhancing the quality of life for affected individuals and their families.

Literatures Citing This Work ​

  1. Alzheimer 100--highlights in the history of Alzheimer research. - K A Jellinger - Journal of neural transmission (Vienna, Austria : 1996) (2006)
  2. X-linked mental retardation and epigenetics. - Guy Froyen;Marijke Bauters;Thierry Voet;Peter Marynen - Journal of cellular and molecular medicine (2006)
  3. A fruitfly's guide to keeping the brain wired. - Maarten Leyssen;Bassem A Hassan - EMBO reports (2007)
  4. Properties of glutamate receptors of Alzheimer's disease brain transplanted to frog oocytes. - Annalisa Bernareggi;Zulma Dueñas;Jorge Mauricio Reyes-Ruiz;Fabio Ruzzier;Ricardo Miledi - Proceedings of the National Academy of Sciences of the United States of America (2007)
  5. Reelin depletion in the entorhinal cortex of human amyloid precursor protein transgenic mice and humans with Alzheimer's disease. - Jeannie Chin;Catherine M Massaro;Jorge J Palop;Myo T Thwin;Gui-Qiu Yu;Nga Bien-Ly;Aaron Bender;Lennart Mucke - The Journal of neuroscience : the official journal of the Society for Neuroscience (2007)
  6. Inhibition of mitogen-activated protein kinase and stimulation of Akt kinase signaling pathways: Two approaches with therapeutic potential in the treatment of neurodegenerative disease. - Robert E Burke - Pharmacology & therapeutics (2007)
  7. APP locus duplication in a Finnish family with dementia and intracerebral haemorrhage. - A Rovelet-Lecrux;T Frebourg;H Tuominen;K Majamaa;D Campion;A M Remes - Journal of neurology, neurosurgery, and psychiatry (2007)
  8. Ten commandments for the future of ageing research in the UK: a vision for action. - Oscar H Franco;Thomas B L Kirkwood;Jonathan R Powell;Michael Catt;James Goodwin;Jose M Ordovas;Frans van der Ouderaa - BMC geriatrics (2007)
  9. G-CSF rescues the memory impairment of animal models of Alzheimer's disease. - Kuen-Jer Tsai;Yueh-Chiao Tsai;Che-Kun James Shen - The Journal of experimental medicine (2007)
  10. Effect of HMG-CoA reductase inhibitors on beta-amyloid peptide levels: implications for Alzheimer's disease. - Kina Höglund;Kaj Blennow - CNS drugs (2007)

... (1220 more literatures)

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