Prenatal Exposures Associated with Neurodevelopmental Delay and Disabilities

Diav–Citrin, Orna

doi:10.1002/ddrr.1102

Cited by 15 publications

(10 citation statements)

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“…The prenatal and early postnatal periods present a time when the developing brain is most susceptible to teratogens such as infectious agents, drugs and substances of abuse (Diav‐Citrin, ; Minnes et al ., ). Clinical studies suggest that maternal Cannabis exposure leads to negative effects on impulsivity, executive function and to increased likelihood of early tobacco and Cannabis use later in life (Minnes et al ., ; Wu et al ., ).…”

Section: Discussionmentioning

confidence: 99%

Long‐term consequences of perinatal fatty acid amino hydrolase inhibition

Morgan

Jew

et al. 2014

British J Pharmacology

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Background and Purpose Fatty acid amide hydrolase inhibitors show promise as a treatment for anxiety, depression and pain. Here we investigated whether perinatal exposure to URB597, a fatty acid amide hydrolase inhibitor, alters brain development and affects behaviour in adult mice. Experimental Approach Mouse dams were treated daily from gestational day 10.5 to 16.5 with 1, 3 or 10 mg kg−1 URB597. MS was used to measure a panel of endocannabinoids and related lipid compounds and brain development was assessed at embryonic day 16.5. Separate cohorts of mouse dams were treated with 10 mg kg−1 URB597, from gestational day 10.5 to postnatal day 7, and the adult offspring were assessed with a battery of behavioural tests. Key Results Perinatal URB597 exposure elevated anandamide and related N‐acyl amides. URB597 did not induce signs of toxicity or affect dam weight gain, neurogenesis or axonal development at embryonic day 16.5. It did lead to subtle behavioural deficits in adult offspring, manifested by reduced cocaine‐conditioned preference, increased depressive behaviours and impaired working memory. Anxiety levels, motor function and sensory‐motor gating were not significantly altered. Conclusions and Implications Taken together, the present results highlight how exposure to elevated levels of anandamide and related N‐acyl amides during brain development can lead to subtle alterations in behaviour in adulthood. Linked Articles This article is part of a themed section on Cannabinoids 2013. To view the other articles in this section visit

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Section: Discussionmentioning

confidence: 99%

Long‐term consequences of perinatal fatty acid amino hydrolase inhibition

Morgan

Jew

et al. 2014

British J Pharmacology

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“…foetal and post‐natal infections, peri‐ and post‐natal neurotoxins and trauma, in utero exposure to alcohol, drugs or environmental chemicals) (see McDermott et al . ; Diav‐Citrin ; Ergaz & Ornoy ; Sansavini et al . ), and corresponding developmental patterns take many forms.…”

Section: Aetiologic Specificitymentioning

confidence: 99%

“…Moreover, the general population of children with developmental delays is highly heterogeneous with many different aetiologies (e.g. foetal and post-natal infections, peri-and post-natal neurotoxins and trauma, in utero exposure to alcohol, drugs or environmental chemicals) (see McDermott et al 2007;Diav-Citrin 2011;Ergaz & Ornoy 2011;Sansavini et al 2011), and corresponding developmental patterns take many forms. Despite the fact that more and more genetic causes of children's delays are being identified (Mefford et al 2012), a precise cause for a substantial number of children cannot yet be established with a reasonable degree of certainty.…”

Section: Aetiologic Specificitymentioning

confidence: 99%

Early Intervention for Children with Intellectual Disabilities: An Update

Guralnick

2016

Research Intellect Disabil

130

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This article provides an update on advances in both developmental and intervention science that have occurred in the field of early intervention for children with developmental delays in the past decade. From the perspective of developmental science, findings related to multiple and reciprocal pathways of influence on the development of children with delays that can inform early intervention practice are discussed. This is followed by a review of two prominent lines of early intervention research: promoting children's developm-ent by enhancing parent-sensitive responsiveness and improving children's cognitive and social outcomes in inclusive preschool settings. Merging policy initiati-ves with our knowledge of developmental processes is discussed as the key to accelerating progress in the development of comprehensive early intervention systems.

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“…The user is also typically unaware that taking vitamin C-containing prepara ons may compromise the results of some medical tests -for example, presence of ascorbic acid and its deriva ves in urine Large doses of deriva ves of re noic acid may be associated with changes in hair colour and texture and hepatotoxicity [1327,1328]. Pregnant women must be especially wary of taking re noids beyond the recommended daily allowance (RDA), as the la er are known to induce differen a on in undifferen ated cells and may cause inborn anomalies and/or developmental delay in the child [1329]. The la er is the main reason for advising against ge ng pregnant during treatments with topical prepara ons including isotre noin (Accutane, for treatment of recalcitrant acne) or etre nate (Tegason, for topical treatment in psoriasis) and in the post-treatment period (up to 2 years a er discon nua on of the use of the re noid) [1330,1331. Vitamin D3 is o en included in prepara ons containing calcium, which is typically jus fied by sta ng that vitamin D3 'assisted the absorp on of calcium'.…”

Section: S Snegov the Experiments Of Professor Bran Ng (1977)mentioning

confidence: 99%

DNA repair systems

Chakarov¹,

Petkova²,

Russev³

2014

Biodiscovery

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This paper provides detailed insight into the mechanisms of repair of different types of DNA damage and the direct molecular players (enzymes repairing the damage or tagging the damaged site for further processing; damage sensor molecules; other signalling and effector molecules). The gene c bases of diseases and condi ons associated with defec ve DNA repair are comprehensively reviewed, from the 'classic' severe diseases such as xeroderma pigmentosum and Cockayne syndrome to the much more subtle UV sensi vity syndromes. The review analyses the basic molecular mechanisms underlying the rela vely rare monogenic diseases of DNA repair and management of genome integrity as well as the common mul factorial diseases and condi ons with late onset that are associated with increased levels of oxida ve stress (metabolic syndrome, diabetes type 2, cardiovascular disease) and with accumula on of 'errors' in DNA (normal and pathological ageing phenotypes, various cancers). The role of cell cycle checkpoints in dividing cells and the mechanisms of decision-making for the fate of a damaged cell are discussed with regards to the cell homeostasis in normal and cancerous ssues. The role of major DNA damageassociated signalling and effector molecules (p53, ATM, poly-(ADP-ribose)-polymerase, DNA-dependent protein kinase, BRCA proteins, re noblastoma protein, and others) is discussed and illustrated with examples in the context of health and disease. DNA repair and programmed cell death are viewed together as a unified mechanism for limi ng the presence of damaged cells and cells with poten ally oncogenic transforma on in mul cellular organisms. Special a en on is paid to ageing as a natural phenomenon and an adap ve evolu onary mechanism, with a brief outline of 'successful ageing'. The differen al rates of repair of DNA in transcribed and nontranscribed regions of the genome and the specifici es of DNA repair profile in some types of cells (terminally differen ated cells, pluripotent stem cells, etc.) and in certain taxonomic groups (e.g. 'the rodent repairadox') are discussed with regards to replica ve ageing and the evolu onary processes on microand macroscale. The role of mutagenesis as a 'hit and miss' mechanism and the 'leakiness' of DNA repair for increasing gene c diversity in the course of individual life and on evolu onary scale and the phenomenology of ongoing molecular evolu on are extensively reviewed. Conflict of Interests:No poten al conflict of interest was disclosed by any of the authors. Types of DNA repair systemsIf you wish for peace, prepare for war.Publius Flavius Vege us Renatus, De Re Militari (circa 380 AD).DNA damage is a very broad term, encompassing many different types of lesions in DNA.Accordingly, DNA repair comprises many different types of pathways and mechanisms covering virtually every possible type of injury to the sequence or the structure of DNA.Accep ng Lewin's defini on of DNA damage "... any change that introduces a devia on from the usual double-helical structure" [1] , we may pre...

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Prenatal Exposures Associated with Neurodevelopmental Delay and Disabilities

Cited by 15 publications

References 182 publications

Long‐term consequences of perinatal fatty acid amino hydrolase inhibition

Long‐term consequences of perinatal fatty acid amino hydrolase inhibition

Early Intervention for Children with Intellectual Disabilities: An Update

DNA repair systems

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