PMID- 20218978
OWN - NLM
STAT- MEDLINE
DCOM- 20100730
LR  - 20181113
IS  - 1476-5381 (Electronic)
IS  - 0007-1188 (Print)
IS  - 0007-1188 (Linking)
VI  - 159
IP  - 8
DP  - 2010 Apr
TI  - Soluble beta amyloid(1-42): a critical player in producing behavioural and 
      biochemical changes evoking depressive-related state?
PG  - 1704-15
LID - 10.1111/j.1476-5381.2010.00669.x [doi]
AB  - BACKGROUND AND PURPOSE: Depression is common in early phases of Alzheimer's 
      disease (AD) and may represent prodromal symptoms of dementia. Recent reports 
      suggest that early memory deficits and neuropsychiatric symptoms are caused by 
      soluble rather than aggregated betaamyloid (Abeta). Thus, we investigated the 
      effects of soluble Abeta(1-42) on working memory and depressive/anxiety-related 
      behaviour in rats and on 5-hydroxytryptaminergic neurotransmission and 
      neurotrophin content in various brain regions. EXPERIMENTAL APPROACH: Behavioural 
      reactivity to novel object recognition, open field, elevated plus maze and forced 
      swimming test were assessed 7 days after i.c.v. injection of Abeta(1-42) or its 
      vehicle. BDNF (brain-derived neurotrophic factor) and NGF (nerve growth factor) 
      mRNA and protein levels and 5-hydroxytriptamine (5-HT) content were measured in 
      the prefrontal cortex (PFC), striatum (STR) and nucleus accumbens (NAc). KEY 
      RESULTS: Abeta(1-42) did not affect the ability to distinguish between familiar 
      and novel objects, but Abeta-treated rats exhibited an increase in forced 
      swimming immobility. No differences were revealed between experimental groups in 
      the elevated plus maze test or in self-grooming (evaluated in the open field). In 
      the PFC, but not STR or NAc, Abeta-injected rats exhibited a selective reduction 
      in 5-HT content, BDNF and NGF expression. CONCLUSIONS AND IMPLICATIONS: Our data 
      suggest that soluble Abeta-treated rats have a depressive, but not 
      anxiogenic-like, profile, accompanied by brain region-dependent alterations in 
      the expression of neurotrophins and 5-hydroxytryptaminergic neurotransmission. 
      Hence, these alterations induced by soluble Abeta might be sensitive indicators 
      of early phases of AD and possible risk factors for the expression of 
      neuropsychiatric symptoms in AD.
FAU - Colaianna, M
AU  - Colaianna M
AD  - Department of Biomedical Sciences, University of Foggia, Italy.
FAU - Tucci, P
AU  - Tucci P
FAU - Zotti, M
AU  - Zotti M
FAU - Morgese, M G
AU  - Morgese MG
FAU - Schiavone, S
AU  - Schiavone S
FAU - Govoni, S
AU  - Govoni S
FAU - Cuomo, V
AU  - Cuomo V
FAU - Trabace, L
AU  - Trabace L
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20100309
PL  - England
TA  - Br J Pharmacol
JT  - British journal of pharmacology
JID - 7502536
RN  - 0 (Amyloid beta-Peptides)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (DNA Primers)
RN  - 0 (Peptide Fragments)
RN  - 0 (amyloid beta-protein (1-42))
RN  - 333DO1RDJY (Serotonin)
RN  - 9061-61-4 (Nerve Growth Factor)
SB  - IM
CIN - Br J Pharmacol. 2010 Oct;161(4):768-70. PMID: 21105218
MH  - Amyloid beta-Peptides/administration & dosage/*pharmacology
MH  - Animals
MH  - Base Sequence
MH  - Behavior, Animal/*drug effects
MH  - Brain-Derived Neurotrophic Factor/genetics/metabolism
MH  - DNA Primers
MH  - Depression/*chemically induced
MH  - Injections, Intraventricular
MH  - Male
MH  - Maze Learning
MH  - Nerve Growth Factor/genetics/metabolism
MH  - Peptide Fragments/administration & dosage/*pharmacology
MH  - Rats
MH  - Rats, Wistar
MH  - Serotonin/metabolism
PMC - PMC2925493
EDAT- 2010/03/12 06:00
MHDA- 2010/07/31 06:00
PMCR- 2011/04/01
CRDT- 2010/03/12 06:00
PHST- 2010/03/12 06:00 [entrez]
PHST- 2010/03/12 06:00 [pubmed]
PHST- 2010/07/31 06:00 [medline]
PHST- 2011/04/01 00:00 [pmc-release]
AID - BPH669 [pii]
AID - 10.1111/j.1476-5381.2010.00669.x [doi]
PST - ppublish
SO  - Br J Pharmacol. 2010 Apr;159(8):1704-15. doi: 10.1111/j.1476-5381.2010.00669.x. 
      Epub 2010 Mar 9.