Amyloid-β oligomers link depressive-like behavior and cognitive deficits in mice

Ledo, José Henrique; Clarke, Julia R.; Ribeiro, Felipe C.; Figueiredo, Cláudia P.; Foguel, Débora; Felice, Fernanda G. De; Ferreira, Sérgio T.

doi:10.1038/mp.2012.168

Cited by 140 publications

(117 citation statements)

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“…In addition, the evidence that implicates PrP C as a binding partner of A␤ peptide oligomers (37) extends the potential relevance of our data to neuropsychiatric manifestations of Alzheimer disease (105). Indeed, the behavioral deficits that indicate a depressive-like behavior of PrP C -null animals are reminiscent of those described in mice subject to injections of A␤ peptide oligomers (106). Further to the importance to specific neurodegenerative diseases, modulation of monoaminergic neurotransmission by PrP C may also be a potential target in major depression and related disorders.…”

Section: Discussionmentioning

confidence: 48%

Prion Protein Modulates Monoaminergic Systems and Depressive-like Behavior in Mice

Beckman

Santos

Americo

et al. 2015

Journal of Biological Chemistry

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Background:The prion protein (PrP C ) functions as a scaffold for cell surface signaling systems, and plays a role in neurodegenerative diseases that include clinical depression among their symptoms. Results: PrP C -null mice showed depressive-like behavior concomitant with functional changes in monoaminergic systems. Conclusion: PrP C regulates functions of monoaminergic synapses. Significance: PrP C may be involved in major depression and related neuropsychiatric disorders.

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Section: Discussionmentioning

confidence: 48%

Prion Protein Modulates Monoaminergic Systems and Depressive-like Behavior in Mice

Beckman

Santos

Americo

et al. 2015

Journal of Biological Chemistry

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“…A pre-clinical study has shown that beta-amyloid oligomers leads to memory impairment and depressive-like behavior in mice (Ledo et al 2013).…”

Section: Bipolar Disorder and Depressionmentioning

confidence: 99%

Alzheimer´s Disease associated with Psychiatric Comorbidities

Garcez

Falchetti

Mina

et al. 2015

An. Acad. Bras. Ciênc.

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Alzheimer's disease (AD) is the most common cause of dementia and has become a severe public health issue. It is estimated that globally, 35.6% of people have some form of dementia. This number is expected to double by 2030, and possibly even triple by 2050. The disease is associated with deficits in cognition/ memory and a reduced ability in coping with everyday life. Moreover, patients can experience behavioral alterations such as mood swings, depression and hallucinations. Therefore, it is common to find the presence of neuropsychiatric comorbidities such as depression, schizophrenia and bipolar disorder during the course or development of AD. These disorders can become severe enough to interfere with the patients daily functioning, and can worsen the course of the disease. However, little is known about the causal relationship between psychiatric comorbidities and AD, or the reasons for the predisposition of some individuals to such disorders. Therefore, the purpose of this review is to clarify the causal relationship between depression, schizophrenia and bipolar disorder with AD.

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“…For example, investigators from Brazil demonstrated that Ab oligomers (AbOs) trigger an inflammatory response in the brain, leading to memory impairment and depressive-like behavior, and that these behaviors can be reversed through the use of the anti-inflammatory drug fluoxetine [35]. They went on to show that AbOs target microglia, the resident immune cells of the central nervous system, stimulating the release of inflammatory cytokines [35]. These studies and others suggest microglia as a promising therapeutic target for AD [36].…”

Section: Developing Therapies For Admentioning

confidence: 99%