RT Book, Section
A1 Seeley, William W.
A1 Miller, Bruce L.
A2 Hauser, Stephen L.
A2 Josephson, S. Andrew
SR Print(0)
ID 1145769546
T1 ALZHEIMER’S DISEASE AND OTHER DEMENTIAS
T2 Harrison's Neurology in Clinical Medicine, 4e
YR 2018
FD 2018
PB McGraw-Hill Education
PP New York, NY
SN 9781259835865
LK neurology.mhmedical.com/content.aspx?aid=1145769546
RD 2024/04/19
AB Approximately  10%  of  all  persons  over  the  age  of  70  years  have  significant  memory  loss,  and  in  more  than  half,  the  cause  is  Alzheimer’s  disease  (AD).  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  young  as  the  third  decade,  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  that  evolves  over  years.  In  typical  amnestic  AD,  brain  imaging  reveals  atrophy  that  begins  in  the  medial  temporal  lobes  before  spreading  to  lateral  and  medial  parietal  and  temporal  lobes  and  lateral  frontal  cortex.  Microscopically,  there  are  neuritic  plaques  containing  amyloid  beta  (Aβ),  neurofibrillary  tangles  (NFTs)  composed  of  hyperphosphorylated  tau  filaments,  and  Aβ  accumulation  of  in  blood  vessel  walls  in  cortex  and  leptomeninges  (see  “Pathology,”  below).  The  identification  of  causative  mutations  and  susceptibility  genes  for  AD  has  provided  a  foundation  for  rapid  progress  in  understanding  the  biological  basis  of  the  disorder.  The  major  genetic  risk  for  AD  is  apolipoprotein  ε4  (Apo  ε4).  Carrying  one  Ε4  allele  increases  the  risk  for  AD  by  2-  to  3-fold,  whereas  two  alleles  increase  the  risk  16-fold.