TY  - CHAP
M1  - Book, Section
TI  - Alzheimer’s Disease
A1  - Rabinovici, Gil D.
A1  - Seeley, William W.
A1  - Miller, Bruce L.
A2  - Loscalzo, Joseph
A2  - Fauci, Anthony
A2  - Kasper, Dennis
A2  - Hauser, Stephen
A2  - Longo, Dan
A2  - Jameson, J. Larry
Y1  - 2022
N1  - 
T2  - Harrison's Principles of Internal Medicine, 21e
AB  - Approximately  50  million  people  across  the  world  are  living  with  dementia.  Alzheimer’s  disease  (AD)  is  the  most  common  cause  of  dementia,  contributing  to  an  estimated  60–70%  of  all  cases.  It  is  estimated  that  the  median  annual  total  cost  of  caring  for  a  single  patient  with  advanced  AD  is  >$50,000,  while  the  emotional  toll  for  family  members  and  caregivers  is  immeasurable.  AD  can  manifest  as  early  as  the  third  decade  of  life,  but  it  is  the  most  common  cause  of  dementia  in  the  elderly.  Patients  most  often  present  with  an  insidious  loss  of  episodic  memory  followed  by  a  slowly  progressive  dementia.  In  typical  amnestic  AD,  brain  atrophy  begins  in  the  medial  temporal  lobes  before  spreading  to  the  inferior  temporal,  lateral,  medial  parietal,  and  dorsolateral  frontal  cortices.  Microscopically,  there  are  widespread  neuritic  plaques  containing  amyloid  beta  (Aβ),  neurofibrillary  tangles  (NFTs)  composed  of  hyperphosphorylated  tau  filaments,  and  Aβ  accumulation  in  blood  vessel  walls  in  cortex  and  leptomeninges  (amyloid  angiopathy,  see  “Pathology,”  below).  The  identification  of  causative  mutations  and  susceptibility  genes  for  AD  has  provided  a  foundation  for  progress  in  understanding  the  biologic  basis  of  the  disorder.  The  major  genetic  risk  factor  for  AD  is  the  ε4  allele  of  the  apolipoprotein  E  (ApoE)  gene.  Carrying  one  ε4  allele  increases  the  risk  for  AD  by  two-  to  threefold  in  women  whereas  carrying  two  alleles  increases  the  risk  ten-  to  fifteenfold  in  both  sexes.  Rapid  progress  in  the  development  of  imaging,  cerebrospinal  fluid  (CSF),  and  plasma  biomarkers  of  Aβ  and  phosphorylated  tau  has  enabled  detection  of  AD  pathologic  hallmarks  in  living  people,  opening  the  door  to  early  detection  and  intervention  with  biologically  specific  therapies.  
SN  - 
PB  - McGraw-Hill Education
CY  - New York, NY
Y2  - 2024/04/17
UR  - accessmedicine.mhmedical.com/content.aspx?aid=1207106940
ER  -