PMID- 26485083
OWN - NLM
STAT- MEDLINE
DCOM- 20160801
LR  - 20160420
IS  - 1471-4159 (Electronic)
IS  - 0022-3042 (Linking)
VI  - 136
IP  - 2
DP  - 2016 Jan
TI  - Glial fibrillar acidic protein in the cerebrospinal fluid of Alzheimer's disease, 
      dementia with Lewy bodies, and frontotemporal lobar degeneration.
PG  - 258-61
LID - 10.1111/jnc.13399 [doi]
AB  - Biomarkers in the cerebrospinal fluid (CSF) are currently regarded as 
      indispensable indicators for accurate differential diagnosis of neurodegenerative 
      disorders. Although high levels of astrocyte-secreted glial fibrillar acidic 
      protein (GFAP) in the CSF of patients with Alzheimer's disease (AD) have been 
      reported, the levels of GFAP in the CSF have not been fully investigated in other 
      neurological disorders that cause dementia, such as dementia with Lewy bodies 
      (DLB) and frontotemporal lobar degeneration (FTLD). In this study, we determined 
      the levels of GFAP in the CSF of healthy control subjects and AD, DLB, and FTLD 
      patients to address two questions: (i) Do the levels of GFAP differ among these 
      disorders? and (ii) Can GFAP be used as a biomarker for the differential 
      diagnosis of these neurodegenerative disorders? The levels of GFAP in AD, DLB, 
      and FTLD patients were significantly higher than those in the healthy control 
      subjects. Although the levels of GFAP were not significantly different between AD 
      and DLB patients, a higher level of GFAP was observed in FTLD patients than in AD 
      and DLB patients. It is concluded that representative neurological disorders 
      causing dementia were associated with higher levels of GFAP in the CSF. We 
      propose the following mechanism concerning the amount of glial fibrillar acidic 
      protein (GFAP) in the cerebrospinal fluid (CSF) in Alzheimer's disease (AD), 
      dementia with Lewy bodies (DLB), and frontotemporal lobar degeneration (FTLD). 
      The increase in the release of GFAP into CSF is considered to reflect the sum of 
      degeneration of astrocytes and astrocytosis. The sum of degeneration and 
      astrocytosis or the GFAP release could be in the order of FTLD > DLB > AD > 
      normal condition.
CI  - (c) 2015 International Society for Neurochemistry.
FAU - Ishiki, Aiko
AU  - Ishiki A
AD  - Department of Geriatrics and Gerontology, Division of Brain Sciences, Institute 
      of Development, Aging and Cancer, Tohoku University, Sendai, Japan.
FAU - Kamada, Maki
AU  - Kamada M
AD  - Department of Geriatrics and Gerontology, Division of Brain Sciences, Institute 
      of Development, Aging and Cancer, Tohoku University, Sendai, Japan.
FAU - Kawamura, Yuki
AU  - Kawamura Y
AD  - Department of Geriatrics and Gerontology, Division of Brain Sciences, Institute 
      of Development, Aging and Cancer, Tohoku University, Sendai, Japan.
FAU - Terao, Chiaki
AU  - Terao C
AD  - Department of Geriatrics and Gerontology, Division of Brain Sciences, Institute 
      of Development, Aging and Cancer, Tohoku University, Sendai, Japan.
FAU - Shimoda, Fumiko
AU  - Shimoda F
AD  - Department of Geriatrics and Gerontology, Division of Brain Sciences, Institute 
      of Development, Aging and Cancer, Tohoku University, Sendai, Japan.
FAU - Tomita, Naoki
AU  - Tomita N
AD  - Department of Geriatrics and Gerontology, Division of Brain Sciences, Institute 
      of Development, Aging and Cancer, Tohoku University, Sendai, Japan.
FAU - Arai, Hiroyuki
AU  - Arai H
AD  - Department of Geriatrics and Gerontology, Division of Brain Sciences, Institute 
      of Development, Aging and Cancer, Tohoku University, Sendai, Japan.
FAU - Furukawa, Katsutoshi
AU  - Furukawa K
AD  - Department of Geriatrics and Gerontology, Division of Brain Sciences, Institute 
      of Development, Aging and Cancer, Tohoku University, Sendai, Japan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20151111
PL  - England
TA  - J Neurochem
JT  - Journal of neurochemistry
JID - 2985190R
RN  - 0 (Amyloid beta-Peptides)
RN  - 0 (Glial Fibrillary Acidic Protein)
RN  - 0 (Peptide Fragments)
RN  - 0 (amyloid beta-protein (1-40))
RN  - 0 (amyloid beta-protein (1-42))
RN  - 0 (tau Proteins)
SB  - IM
MH  - Aged
MH  - Alzheimer Disease/*cerebrospinal fluid
MH  - Amyloid beta-Peptides/cerebrospinal fluid
MH  - Analysis of Variance
MH  - Female
MH  - Frontotemporal Lobar Degeneration/*cerebrospinal fluid
MH  - Glial Fibrillary Acidic Protein/*cerebrospinal fluid
MH  - Humans
MH  - Lewy Body Disease/*cerebrospinal fluid
MH  - Male
MH  - Mental Status Schedule
MH  - Peptide Fragments/cerebrospinal fluid
MH  - tau Proteins/cerebrospinal fluid
OTO - NOTNLM
OT  - Alzheimer's disease
OT  - cerebrospinal fluid
OT  - dementia with Lewy bodies
OT  - frontotemporal lobar degeneration
OT  - glial fibrillar acidic protein
EDAT- 2015/10/21 06:00
MHDA- 2016/08/02 06:00
CRDT- 2015/10/21 06:00
PHST- 2015/06/02 00:00 [received]
PHST- 2015/10/08 00:00 [revised]
PHST- 2015/10/09 00:00 [accepted]
PHST- 2015/10/21 06:00 [entrez]
PHST- 2015/10/21 06:00 [pubmed]
PHST- 2016/08/02 06:00 [medline]
AID - 10.1111/jnc.13399 [doi]
PST - ppublish
SO  - J Neurochem. 2016 Jan;136(2):258-61. doi: 10.1111/jnc.13399. Epub 2015 Nov 11.