RT Book, Section
A1 Mosconi, Tony
A1 Graham, Victoria
SR Print(0)
ID 1148430505
T1 Diencephalon
T2 Neuroscience for Rehabilitation
YR 2017
FD 2017
PB McGraw-Hill Education
PP New York, NY
SN 9780071828888
LK accessphysiotherapy.mhmedical.com/content.aspx?aid=1148430505
RD 2024/04/19
AB >  CASE  9Alzheimer's  DiseaseNorma  B.  was  shocked  when  the  doctor  gave  her  the  diagnosis  of  mild,  late  onset  Alzheimer's  disease  (AD)  at  age  91.  Her  husband  Georg  was  not;  it  explained  her  increasingly  strange  behavior  over  the  past  few  years.  She  had  been  ever  more  dependent  on  him  for  names  and  details  of  events,  repeating  the  same  information  several  times  in  a  short  period,  misplacing  kitchen  and  other  items,  and  losing  hundreds  of  dollars.They  phoned  each  of  their  grown  children  to  share  the  sad  news.  They  were  determined  that  this  would  not  change  their  lives.  In  fact,  Georg  became  more  patient  now  that  he  understood  Norma's  behavior.  Georg  and  Norma  had  only  just  found  each  other  again,  college  sweethearts  reunited  in  their  70s  after  a  lifetime  apart.  Norma  admitted  to  her  daughter  the  early  difficulties:  “It's  really  hard  because  I’m  losing  my  friendships.”  She  told  her,  “I  feel  lonely;  I  can’t  talk  to  them  because  I  forget  the  words.  They  are  so  kind  and  make  an  effort  to  include  me,  but  I’m  ashamed.  It's  embarrassing.”Late-onset  Alzheimer's  disease,  the  most  common  form,  begins  with  age-related  free  radicals,  generated  in  the  mitochondria,  cause  oxidative  stress  which  further  damages  the  mitochondria,  disrupting  ATP  production.  With  loss  of  ATP  to  fuel  maintenance  of  the  membrane  resting  potential,  the  disrupted  mitochondrial  cell  membrane  becomes  permeable  to  an  influx  of  damaging  levels  of  calcium  while  leaking  large  proteins  into  the  surrounding  cell.  Leaked  proteins  are  neurotoxic  and  produce  senile  plaques  and  neurofibrillary  tangles,  two  pathological  findings  in  AD.  Senile  plaques  are  extracellular  deposition  of  beta  amyloid-Aβ,  causing  neuron  death,  synapse  damage,  and  loss  of  long-term  potentiation.  New  diffusion  tensor  imaging  to  view  white  matter  axon  tracts  reveals  selective  early  degeneration  within  the  limbic–diencephalic  network.  This  causes  early  disruption  in  memory,  behavior,  and  emotion  due,  in  part,  to  loss  of  acetylcholinergic  cells.  MRI  imaging  shows  selective  early  damage  from  plaques  to  the  entorhinal  cortex  and  hippocampus,  disrupting  path-finding  directionality  (such  as  whether  to  turn  left  or  right)  and  memory  loss.  Secondary  damage  from  intracellular  accumulation  of  tau  protein  disrupts  axon  transport  and  is  found  extracellularly  in  neurofibrillary  tangles.  Abnormal  tau  first  appears  in  the  entorhinal  cortex,  then  in  the  hippocampus,  and  at  later  stages  in  the  association  cortex.Norma's  clinical  findings  were  consistent  with  the  early  damage  to  the  limbic  system  pathways  involving  memory,  behavior,  and  emotions.  Her  symptoms  progressed  very  slowly  over  the  next  few  years.  She  was  the  choir  director  at  their  church,  and  when  this  became  too  difficult  to  manage,  she  cut  back  to  just  playing  the  piano  during  service,  which  remained  easy  due  to  years  of  practice.  However,  she  noticed  that  she  would  forget  the  song  order  and  constantly  have  to  check  the  printed  schedule,  something  that  had  never  happened  before.  She  became  focused  on  earlier  events  in  her  own  life  as  recent  memory  faded;  she  replaced  the  photos  of  her  grandchildren  with  a  photo  of  her  own  grandfather.  She  no  longer  recognized  or  even  thought  of  her  own  grandchildren  in  her  daily  life.  Over  time,  ...