PMID- 17548170
OWN - NLM
STAT- MEDLINE
DCOM- 20080103
LR  - 20151119
IS  - 0306-9877 (Print)
IS  - 0306-9877 (Linking)
VI  - 69
IP  - 6
DP  - 2007
TI  - Glatiramer acetate could be a potential therapeutic agent for Parkinson's disease 
      through its neuroprotective and anti-inflammatory effects.
PG  - 1219-21
AB  - Parkinson's disease (PD) is the second most common neurodegenerative disease 
      after Alzheimer's disease. The hallmark pathologic feature of PD is dopamine 
      deficiency, caused by the degeneration of nigrostriatal dopaminergic neurons. 
      Current treatments for PD mainly address the dopaminergic features of the 
      disease; however they do not modify the progression of neurodegeneration. The 
      need for newer and more effective agents is consequently receiving a great deal 
      of attention. Brain-derived neurotrophic factor (BDNF), a member of the 
      neurotrophic factor family, can promote survival of injured dopaminergic 
      nigrostriatal neurons in the rodent. Postmortem studies have suggested that BDNF 
      deficiency may play a role in PD pathogenesis. This is further supported by the 
      finding that BDNF administration has a therapeutic effect in animal models of PD. 
      Glatiramer acetate (GA) is a collection of synthetic polypeptides approved for 
      the treatment of relapsing-remitting multiple sclerosis. Preclinical studies have 
      demonstrated that peripheral GA administration can enhance central BDNF activity 
      and augment neurogenesis. Furthermore, PD has been associated with an 
      inflammatory process in the brain. Animal studies have demonstrated that GA 
      administration has a central anti-inflammatory effect through the release of 
      anti-inflammatory cytokines. From the above evidence, GA could act as a potential 
      therapeutic agent for PD by increasing central BDNF and by exerting an 
      anti-inflammatory effect. With the recent finding that GA administration can 
      prevent neuronal loss and cognitive decline in Alzheimer's disease 
      double-transgenic mice, early GA treatment may also prevent neurodegeneration and 
      manifestations of PD symptoms in subjects with familial Parkinson's disease.
FAU - Tsai, Shih-Jen
AU  - Tsai SJ
AD  - Department of Psychiatry, Taipei Veterans General Hospital, No. 201 Shih-Pai 
      Road, Sec. 2, 11217 Taipei, Taiwan sjtsai@vghtpe.gov.tw
LA  - eng
PT  - Journal Article
DEP - 20070604
PL  - United States
TA  - Med Hypotheses
JT  - Medical hypotheses
JID - 7505668
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Cytokines)
RN  - 0 (Immunosuppressive Agents)
RN  - 0 (Peptides)
RN  - 5M691HL4BO (Glatiramer Acetate)
RN  - VTD58H1Z2X (Dopamine)
SB  - IM
MH  - Alzheimer Disease/pathology/therapy
MH  - Animals
MH  - Anti-Inflammatory Agents/*pharmacology
MH  - Brain/metabolism
MH  - Brain-Derived Neurotrophic Factor/*administration & dosage
MH  - Cytokines/metabolism
MH  - Dopamine/deficiency/metabolism
MH  - Glatiramer Acetate
MH  - Immunosuppressive Agents/*therapeutic use
MH  - Inflammation
MH  - Mice
MH  - Mice, Transgenic
MH  - Models, Theoretical
MH  - Neurons/metabolism
MH  - Parkinson Disease/*drug therapy/pathology
MH  - Peptides/chemistry/*pharmacology
EDAT- 2007/06/06 09:00
MHDA- 2008/01/04 09:00
CRDT- 2007/06/06 09:00
PHST- 2007/04/05 00:00 [received]
PHST- 2007/04/05 00:00 [accepted]
PHST- 2007/06/06 09:00 [pubmed]
PHST- 2008/01/04 09:00 [medline]
PHST- 2007/06/06 09:00 [entrez]
AID - S0306-9877(07)00294-0 [pii]
AID - 10.1016/j.mehy.2007.04.014 [doi]
PST - ppublish
SO  - Med Hypotheses. 2007;69(6):1219-21. doi: 10.1016/j.mehy.2007.04.014. Epub 2007 
      Jun 4.