Book contents
- Frontmatter
- Contents
- List of contributors
- Preface
- Section I Schizophrenia
- Section II Mood Disorders
- Section III Anxiety Disorders
- Section IV Cognitive Disorders
- 23 Structural imaging of Alzheimer's disease
- 24 Functional imaging of Alzheimer's disease
- 25 Molecular imaging of Alzheimer's disease
- 26 Neuroimaging of Parkinson's disease
- 27 Neuroimaging of other dementing disorders
- 28 Neuroimaging of cognitive disorders: commentary
- Section V Substance Abuse
- Section VI Eating Disorders
- Section VII Developmental Disorders
- Index
- References
24 - Functional imaging of Alzheimer's disease
from Section IV - Cognitive Disorders
Published online by Cambridge University Press: 10 January 2011
- Frontmatter
- Contents
- List of contributors
- Preface
- Section I Schizophrenia
- Section II Mood Disorders
- Section III Anxiety Disorders
- Section IV Cognitive Disorders
- 23 Structural imaging of Alzheimer's disease
- 24 Functional imaging of Alzheimer's disease
- 25 Molecular imaging of Alzheimer's disease
- 26 Neuroimaging of Parkinson's disease
- 27 Neuroimaging of other dementing disorders
- 28 Neuroimaging of cognitive disorders: commentary
- Section V Substance Abuse
- Section VI Eating Disorders
- Section VII Developmental Disorders
- Index
- References
Summary
Alzheimer's disease
Background
Alzheimer's disease (AD) is a devastating progressive neurodegenerative disorder that is the most common cause of age-related dementia, accounting for between 60 and 80% of cases of dementia. In 2008, around 5.2 million Americans had AD, with an approximate annual cost of $100 billion. It is estimated that between 11 and 16 million people will be diagnosed with AD in the United States by 2050 (Alzheimer's Association, 2008).
Neuropathological alterations in AD include synaptic loss and cortical atrophy, buildup of beta-amyloid fragments into the “senile” plaques between neurons identified a century ago, and of tau protein into the hallmark neurofibrillary tangles within dead or dying neurons. Cholinergic and glutaminergic pathways are prominently involved in the pathophysiology of AD. While the genetic bases of sporadic late-onset AD are not yet well understood, there are several genetic factors that have been identified as playing a role in the disease. A small number of AD cases (<5%) are familial in nature and caused by rare mutations in the amyloid precursor protein (APP) or presenilin (PSEN) genes. Presence of the ε4 allele of the apolipoprotein-E (APOE) gene confers increased risk of the more prominent late-onset form of AD, and many studies aiming to identify risk markers for AD focus on these genes.
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- Understanding Neuropsychiatric DisordersInsights from Neuroimaging, pp. 332 - 350Publisher: Cambridge University PressPrint publication year: 2010