Abstract
Alzheimer’s disease is a tragic illness that robs the affected individual of their cognitive skills, leading from an initial stage of mild cognitive impairment to progressively severe dementia. Despite being highly prevalent in the geriatric population, there still is no effective treatment that halts the progression of the disease; despite detailed knowledge about the pathophysiology of neurotoxic neurofibrillary plaque and tangle formation, Alzheimer’s disease remains a major cause of dementia that still has no effective treatment. Although medications such as cholinesterase inhibitors can be of mild to moderate help with some of the symptomatic impairments in memory, there is no treatment yet available that addresses the core problem of progressive neuronal dysfunction and cell death. The numbers of affected patients are staggering with more than 35 million worldwide suffering with Alzheimer’s and other dementias; the incidence also doubles for every 5 years after 65 years of age; economic costs of the disease are substantial, and anticipated to exceed $1 trillion by 2050.
This is a preview of subscription content, log in via an institution to check access.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
References
Müller U, Winter P, Graeber MB. A presenilin 1 mutation in the first case of Alzheimer’s disease. Lancet Neurol. 2013;12:129–30.
Rupp C, Beyreuther K, Maurer K, Kins S. A presenilin 1 mutation in the first case of Alzheimer’s disease: revisited. Alzheimers Dement. 2014;10:869–72.
Filley CM, Rollins YD, Anderson CA, et al. The genetics of very early onset Alzheimer disease. Cogn Behav Neurol. 2007;20:149–56.
Graeber MB, Kösel S, Grasbon-Frodl E, et al. Histopathology and APOE genotype of the first Alzheimer disease patient, Auguste D. Neurogenetics. 1998;1:223–8.
Ward A, Crean S, Mercaldi CJ, et al. Prevalence of apolipoprotein E4 genotype and homozygotes (APOE e4/4) among patients diagnosed with Alzheimer’s disease: a systematic review and meta-analysis. Neuroepidemiology. 2012;38(1):1–17.
Ferri CP, Prince M, Brayne C, et al. Global prevalence of dementia: a Delphi consensus study. Lancet. 2005;366(9503):2112–7.
Graeber MB, Kösel S, Egensperger R, et al. Rediscovery of the case described by Alois Alzheimer in 1911: historical, histological and molecular genetic analysis. Neurogenetics. 1997;1:73–80.
Stefanacci RG. The costs of Alzheimer’s disease and the value of effective therapies. Am J Manag Care. 2011;17:S356–62.
Helzner EP, Scarmeas N, Cosentino S, et al. Survival in Alzheimer disease: a multiethnic, population-based study of incident cases. Neurology. 2008;71:1489–95.
Nalivaeva NN, Turner AJ. The amyloid precursor protein: a biochemical enigma in brain development, function and disease. FEBS Lett. 2013;587(13):2046–54.
Satpute-Krishnan P, Degiorgis JA, Conley MP, et al. A peptide zipcode sufficient for anterograde transport within amyloid precursor protein. Proc Natl Acad Sci U S A. 2006;103(44):16532.
Zhou J, Yu Q, Zou T. Alternative splicing of exon 10 in the tau gene as a target for treatment of tauopathies. BMC Neurosci. 2008;9 Suppl 2:S10.
Noda K, Sasaki K, Fujimi K, et al. Quantitative analysis of neurofibrillary pathology in a general population to reappraise neuropathological criteria for senile dementia of the neurofibrillary tangle type (tangle-only dementia): the Hisayama Study. Neuropathology. 2006;26:508–18.
McKee AC, Cantu RC, Nowinski CJ, et al. Chronic traumatic encephalopathy in athletes: progressive tauopathy following repetitive head injury. J Neuropathol Exp Neurol. 2009;68:709–35.
Mosconi L, Mistur R, Switalski R, et al. FDG-PET changes in brain glucose metabolism from normal cognition to pathologically verified Alzheimer’s disease. Eur J Nucl Med Mol Imaging. 2009;36:811–22.
Meyer M, Koeppe RA, Frey KA, Foster NL, Kuhl DE. Positron emission tomography measures of benzodiazepine binding in Alzheimer’s disease. Arch Neurol. 1995;52:314–7.
Ma Y, Zhang S, Li J, et al. Predictive accuracy of amyloid imaging for progression from mild cognitive impairment to Alzheimer disease with different lengths of follow-up: a meta-analysis. [Corrected]. Medicine (Baltimore). 2014;93(27), e150.
Leinonen V, Rinne JO, Virtanen KA, et al. Positron emission tomography with [18F]flutemetamol and [11C]PiB for in vivo detection of cerebral cortical amyloid in normal pressure hydrocephalus patients. Eur J Neurol. 2013;20:1043–52.
Kondo M, Tokuda T, Itsukage M, et al. Distribution of amyloid burden differs between idiopathic normal pressure hydrocephalus and Alzheimer’s disease. Neuroradiol J. 2013;26(1):41–6.
Hamilton R, Patel S, Lee EB, et al. Lack of shunt response in suspected idiopathic normal pressure hydrocephalus with Alzheimer disease pathology. Ann Neurol. 2010;68(4):535–40.
Graff-Radford NR. Alzheimer CSF, biomarkers may be misleading in normal-pressure hydrocephalus. Neurology. 2014;83(17):1573–5.
Author information
Authors and Affiliations
Rights and permissions
Copyright information
© 2016 Springer International Publishing Switzerland
About this chapter
Cite this chapter
Meyer, M.A. (2016). Alzheimer’s Disease. In: Neurologic Disease. Springer, Cham. https://doi.org/10.1007/978-3-319-39581-4_7
Download citation
DOI: https://doi.org/10.1007/978-3-319-39581-4_7
Published:
Publisher Name: Springer, Cham
Print ISBN: 978-3-319-39579-1
Online ISBN: 978-3-319-39581-4
eBook Packages: MedicineMedicine (R0)