PMID- 26138497
OWN - NLM
STAT- MEDLINE
DCOM- 20160322
LR  - 20150703
IS  - 1660-2862 (Electronic)
IS  - 1660-2854 (Linking)
VI  - 15
IP  - 3
DP  - 2015
TI  - Beyond the Hypothesis of Serum Anticholinergic Activity in Alzheimer's Disease: 
      Acetylcholine Neuronal Activity Modulates Brain-Derived Neurotrophic Factor 
      Production and Inflammation in the Brain.
PG  - 182-7
LID - 10.1159/000381531 [doi]
AB  - The brain of Alzheimer's disease (AD) patients is characterized by 
      neurodegeneration, especially an acetylcholine (ACh) neuronal deficit with 
      accumulation of beta-amyloid protein, which leads to oxygen stress and inflammation. 
      The active oxygen directly damages the neuron by increasing intracellular Ca(2+). 
      The inflammation is due to activation of the microglia, thereby producing 
      cytokines which inhibit the production of brain-derived neurotrophic factor 
      (BDNF). As the BDNF acts by neuronal protection, synaptogenesis and neurogenesis, 
      the reduction of BDNF in the brain of AD patients worsens the symptoms of AD. On 
      the other hand, treatment of AD patients with a cholinesterase inhibitor enhances 
      ACh activity and inhibits inflammation. Then the expression of BDNF is restored 
      and neuroprotection reestablished. However, there are several reports which 
      showed controversial results concerning the relationship between BDNF and AD. We 
      speculate that BDNF is related to some neurocognitive process and reflects 
      neuronal activity in other neurodegenerative and neuropsychiatric disorders and 
      that in the mild cognitive impairment stage, BDNF and choline acetyltransferase 
      (ChAT) activities are hyperactivated because of a compensatory mechanism of AD 
      pathology. In contrast, in the mild stage of AD, BDNF and ChAT activity are 
      downregulated.
CI  - (c) 2015 S. Karger AG, Basel.
FAU - Hachisu, Mitsugu
AU  - Hachisu M
AD  - Department of Pharmaceutical Therapeutics, Division of Clinical Pharmacy, School 
      of Pharmacy, Showa University, Tokyo, Japan.
FAU - Konishi, Kimiko
AU  - Konishi K
FAU - Hosoi, Misa
AU  - Hosoi M
FAU - Tani, Masayuki
AU  - Tani M
FAU - Tomioka, Hiroi
AU  - Tomioka H
FAU - Inamoto, Atsuko
AU  - Inamoto A
FAU - Minami, Sousuke
AU  - Minami S
FAU - Izuno, Takuji
AU  - Izuno T
FAU - Umezawa, Kaori
AU  - Umezawa K
FAU - Horiuchi, Kentaro
AU  - Horiuchi K
FAU - Hori, Koji
AU  - Hori K
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20150630
PL  - Switzerland
TA  - Neurodegener Dis
JT  - Neuro-degenerative diseases
JID - 101189034
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Cholinergic Antagonists)
RN  - EC 2.3.1.6 (Choline O-Acetyltransferase)
RN  - N9YNS0M02X (Acetylcholine)
SB  - IM
MH  - Acetylcholine/metabolism
MH  - *Alzheimer Disease/complications/drug therapy/metabolism
MH  - Animals
MH  - Brain/*pathology
MH  - Brain-Derived Neurotrophic Factor/*metabolism
MH  - Choline O-Acetyltransferase/metabolism
MH  - Cholinergic Antagonists/*therapeutic use
MH  - Encephalitis/*etiology
MH  - Humans
MH  - Neurons/drug effects/*metabolism
EDAT- 2015/07/04 06:00
MHDA- 2016/03/24 06:00
CRDT- 2015/07/04 06:00
PHST- 2015/07/04 06:00 [entrez]
PHST- 2015/07/04 06:00 [pubmed]
PHST- 2016/03/24 06:00 [medline]
AID - 000381531 [pii]
AID - 10.1159/000381531 [doi]
PST - ppublish
SO  - Neurodegener Dis. 2015;15(3):182-7. doi: 10.1159/000381531. Epub 2015 Jun 30.