TY - JOUR
T1 - Alzheimer's disease
AU - Masters, Colin L.
AU - Bateman, Randall
AU - Blennow, Kaj
AU - Rowe, Christopher C.
AU - Sperling, Reisa A.
AU - Cummings, Jeffrey L.
N1 - Publisher Copyright:
© 2015 Macmillan Publisher Limited. All rights reserved.
PY - 2015/10/15
Y1 - 2015/10/15
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=85017240652&partnerID=8YFLogxK
U2 - 10.1038/nrdp.2015.56
DO - 10.1038/nrdp.2015.56
M3 - Review article
C2 - 27188934
AN - SCOPUS:85017240652
SN - 2056-676X
VL - 1
JO - Nature Reviews Disease Primers
JF - Nature Reviews Disease Primers
M1 - 15056
ER -