The glial perspective of autism spectrum disorders

Zeidán-Chuliá, Fares; Салмина, А. Б.; Malinovskaya, N. A.; Нода, Мами; Verkhratsky, Alexei; Moreira, José Cláudio Fonseca

doi:10.1016/j.neubiorev.2013.11.008

Cited by 103 publications

(71 citation statements)

References 209 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This PPA-induced astrogliosis is also consistent with previous findings from rats treated with PPA [10,[12][13][14] and in humans with ASD [26][27][28], and may indicate a neuroinflammatory response [12,14,27]. It is interesting to speculate whether this response may have contributed to the social impairments observed [28], however, considering the rapid onset of the social impairments it seems unlikely that the PPA-induced astrogliosis was the mechanism responsible for initiating the social deficits. Rather, they are likely to Fig.…”

Section: Further Support For the Ppa Model Of Asdsupporting

confidence: 88%

Intracerebroventricular injection of propionic acid, an enteric metabolite implicated in autism, induces social abnormalities that do not differ between seizure-prone (FAST) and seizure-resistant (SLOW) rats

Shultz

Aziz

Yang

et al. 2015

Behavioural Brain Research

View full text Add to dashboard Cite

Section: Further Support For the Ppa Model Of Asdsupporting

confidence: 88%

Intracerebroventricular injection of propionic acid, an enteric metabolite implicated in autism, induces social abnormalities that do not differ between seizure-prone (FAST) and seizure-resistant (SLOW) rats

Shultz

Aziz

Yang

et al. 2015

Behavioural Brain Research

View full text Add to dashboard Cite

“…Microglial cells influence numerous physiological processes including neural development, synaptic plasticity, and cognition [29,34]. Also activated microglial cells are known to interact with neurons and participate in the events of synaptic pruning [28,30].…”

Section: Discussionmentioning

confidence: 99%

“…Generally, all CNS diseases involve microglia [28,30], in particular inflammatory diseases such as stroke, multiple sclerosis, neurodegenerative diseases, and after cerebral infection, e.g., with Toxoplasma gondii . Microglial cells also contribute fundamentally to psychiatric disorders such as the autism spectrum disorders [34]. Thus, Tff3 expression in activated microglia opens a plethora of different functions for this peptide in the brain and it will be an important aim for the future to test if Tff3 is expressed also in activated microglial cells in vivo .…”

Section: Discussionmentioning

confidence: 99%

Tff3 is Expressed in Neurons and Microglial Cells

Stellmacher

Znalesniak

et al. 2014

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: The trefoil factor family (TFF) peptide TFF3 is typically secreted by mucous epithelia, but is also expressed in the immune system and the brain. It was the aim of this study to determine the cerebral cell types which express Tff3. Methods: Primary cultures from rat embryonic or neonatal cerebral cortex and hippocampus, respectively, were studied by means of RT-PCR and immunofluorescence. Moreover, Tff3 expression was localized by immunocytochemistry in sections of adult rat cerebellum. Results: Tff3 transcripts were detectable in neural cultures of both the cortex and the hippocampus as well as in glial cell-enriched cultures. Tff3 peptide co-localized with Map2 indicating an expression in neurons in vitro. The neuronal expression was confirmed by immunofluorescence studies of adult rat cerebellum. Furthermore, Tff3 peptide showed also a clear co-localization with Iba-1 in vitro typical of activated microglial cells. Conclusion: The neuronal expression of Tff3 is in line with a function of a typical neuropeptide influencing, e.g., fear, memory, depression and motoric skills. The expression in activated microglial cells, which is demonstrated here for the first time, points towards a possible function for Tff3 in immune reactions in the CNS. This opens a plethora of additional possible functions for Tff3 including synaptic plasticity and cognition as well as during neuroinflammatory diseases and psychiatric disorders.

show abstract

“…In the CNS, there is evidence that microglial cells are also implicated in autism [284, 297-299]. An experimental genetic autism paradigm revealed a transient reduction, during the first postnatal week, of the microglial marker Iba1 in the basolateral amygdala, one of main cerebral regions executing behaviors impaired in ASD [300].…”

Section: Neural and Immune Network Underlying Autismmentioning

confidence: 99%

Neuroimmune and Inflammatory Signals in Complex Disorders of the Central Nervous System

Liberman

Trías

Chagas

et al. 2018

Neuroimmunomodulation

View full text Add to dashboard Cite

An extensive microglial-astrocyte-monocyte-neuronal cross talk seems to be crucial for normal brain function, development, and recovery. However, under certain conditions neuroinflammatory interactions between brain cells and neuroimmune cells influence disease outcome and brain pathology. Microglial cells express a range of functional states with dynamically pleomorphic profiles from a surveilling status of synaptic transmission to an active player in major events of development such as synaptic elimination, regeneration, and repair. Also, inflammation mediates a series of neurotoxic roles in neuropsychiatric conditions and neurodegenerative diseases. The present review discusses data on the involvement of neuroinflammatory conditions that alter neuroimmune interactions in four different pathologies. In the first section of this review, we discuss the ability of the early developing brain to respond to a focal lesion with a rapid compensatory plasticity of intact axons and the role of microglial activation and proinflammatory cytokines in brain repair. In the second section, we present data of neuroinflammation and neurodegenerative disorders and discuss the role of reactive astrocytes in motor neuron toxicity and the progression of amyotrophic lateral sclerosis. In the third section, we discuss major depressive disorders as the consequence of dysfunctional interactions between neural and immune signals that result in increased peripheral immune responses and increase proinflammatory cytokines. In the last section, we discuss autism spectrum disorders and altered brain circuitries that emerge from abnormal long-term responses of innate inflammatory cytokines and microglial phenotypic dysfunctions.

show abstract

The glial perspective of autism spectrum disorders

Cited by 103 publications

References 209 publications

Intracerebroventricular injection of propionic acid, an enteric metabolite implicated in autism, induces social abnormalities that do not differ between seizure-prone (FAST) and seizure-resistant (SLOW) rats

Intracerebroventricular injection of propionic acid, an enteric metabolite implicated in autism, induces social abnormalities that do not differ between seizure-prone (FAST) and seizure-resistant (SLOW) rats

Tff3 is Expressed in Neurons and Microglial Cells

Neuroimmune and Inflammatory Signals in Complex Disorders of the Central Nervous System

Contact Info

Product

Resources

About