Nadia Said, Ph.D.

@article{pmid33648675,

title = {Drug addiction co-morbidity with alcohol: Neurobiological insights},

author = {M Adrienne McGinn and Caroline B Pantazis and Brendan J Tunstall and Renata C N Marchette and Erika R Carlson and Nadia Said and George F Koob and Leandro F Vendruscolo},

url = {https://pubmed.ncbi.nlm.nih.gov/33648675/},

doi = {10.1016/bs.irn.2020.11.002},

issn = {2162-5514},

year  = {2021},

date = {2021-01-01},

urldate = {2021-01-01},

journal = {Int Rev Neurobiol},

volume = {157},

pages = {409--472},

abstract = {Addiction is a chronic disorder that consists of a three-stage cycle of binge/intoxication, withdrawal/negative affect, and preoccupation/anticipation. These stages involve, respectively, neuroadaptations in brain circuits involved in incentive salience and habit formation, stress surfeit and reward deficit, and executive function. Much research on addiction focuses on the neurobiology underlying single drug use. However, alcohol use disorder (AUD) can be co-morbid with substance use disorder (SUD), called dual dependence. The limited epidemiological data on dual dependence indicates that there is a large population of individuals suffering from addiction who are dependent on more than one drug and/or alcohol, yet dual dependence remains understudied in addiction research. Here, we review neurobiological data on neurotransmitter and neuropeptide systems that are known to contribute to addiction pathology and how the involvement of these systems is consistent or divergent across drug classes. In particular, we highlight the dopamine, opioid, corticotropin-releasing factor, norepinephrine, hypocretin/orexin, glucocorticoid, neuroimmune signaling, endocannabinoid, glutamate, and GABA systems. We also discuss the limited research on these systems in dual dependence. Collectively, these studies demonstrate that the use of multiple drugs can produce neuroadaptations that are distinct from single drug use. Further investigation into the neurobiology of dual dependence is necessary to develop effective treatments for addiction to multiple drugs.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid28729061,

title = {Biomarkers for Alzheimer Disease: Classical and Novel Candidates' Review},

author = {Nadia El Kadmiri and Nadia Said and Ilham Slassi and Bouchra El Moutawakil and Sellama Nadifi},

url = {https://pubmed.ncbi.nlm.nih.gov/28729061/},

doi = {10.1016/j.neuroscience.2017.07.017},

issn = {1873-7544},

year  = {2018},

date = {2018-01-01},

urldate = {2018-01-01},

journal = {Neuroscience},

volume = {370},

pages = {181--190},

abstract = {The biomarkers may be useful for predictive diagnosis of Alzheimer's disease (AD). The current challenge is to diagnose it in its preclinical phase. The combination of cerebrospinal fluid (CSF) biomarkers and imaging has been investigated extensively for a number of years. It can provide an increased diagnostic accuracy. This review discusses the contribution of classical biomarkers to predict AD and highlights novel candidates identified as potential markers for AD. We referred to the electronic databases PubMed/Medline and Web of Science to search for articles that were published until February 2016. Sixty-two records were included in qualitative synthesis. In the first section, the results show the contribution of biomarkers to predict and track AD considered as classical biomarkers. In the second section, the results highlight the involvement of novel candidates that should be considered for future evaluation in the characterization of the AD progression. Reported findings open prospect to define noninvasive biomarkers to predict AD before symptoms onset.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid27235743,

title = {Prenatal stress alters diazepam withdrawal syndrome and 5HT1A receptor expression in the raphe nuclei of adult rats},

author = {S Lakehayli and N Said and M El Khachibi and M El Ouahli and S Nadifi and F Hakkou and A Tazi},

url = {https://pubmed.ncbi.nlm.nih.gov/27235743/},

doi = {10.1016/j.neuroscience.2016.05.035},

issn = {1873-7544},

year  = {2016},

date = {2016-01-01},

urldate = {2016-01-01},

journal = {Neuroscience},

volume = {330},

pages = {50--56},

abstract = {Early-life events have long-term effects on brain structures and cause behavioral alterations that persist into adulthood. The present experiments were designed to investigate the effects of prenatal stress on diazepam-induced withdrawal syndrome and serotonin-1A (5HT1A) receptor expression in the raphe nuclei of adult offspring. The results of the present study reveal that maternal exposure to chronic footshock stress increased the anxiety-like behavior in the prenatally stressed (PS) animals withdrawn from chronic diazepam (2.5mg/kg/day i.p for 1week). Moreover, prenatal stress induced a down-regulation of 5HT1A mRNA in the raphe nuclei of adult offspring. To our knowledge, this study is the first to demonstrate that maternal exposure to chronic footshock stress enhances diazepam withdrawal symptoms and alters 5HT1A receptor gene expression in the raphe nuclei of adult offspring. Thus, more studies are needed to clarify the mechanisms underlying the decrease of 5HT1A receptors expression in the raphe nuclei of PS rats.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid26192093,

title = {Prenatal stress induces vulnerability to nicotine addiction and alters D2 receptors' expression in the nucleus accumbens in adult rats},

author = {N Said and S Lakehayli and M El Khachibi and M El Ouahli and S Nadifi and F Hakkou and A Tazi},

url = {https://pubmed.ncbi.nlm.nih.gov/26192093/},

doi = {10.1016/j.neuroscience.2015.07.029},

issn = {1873-7544},

year  = {2015},

date = {2015-09-01},

urldate = {2015-09-01},

journal = {Neuroscience},

volume = {304},

pages = {279--285},

abstract = {Prenatal stress (PS) can induce several long-lasting behavioral and molecular abnormalities in rats. It can also be considered as a risk factor for many psychiatric diseases like schizophrenia, depression or PTSD and predispose to addiction. In this study, we investigated the effect of prenatal stress on the reinforcing properties of nicotine in the CPP paradigm. Then, we examined the mRNA expression of the D2 dopaminergic receptors using the quantitative real-time PCR technique in the nucleus accumbens (NAcc). We found that prenatally stressed rats exhibited a greater place preference for the nicotine-paired compartment than the control rats. Moreover, we observed an overexpression of the DRD2 gene in adult offspring stressed in utero and a downregulation in the PS NIC group (PS rats treated with nicotine) compared with their control counterparts (C NIC). These data suggest that maternal stress can permanently alter the offspring's addictive behavior and D2 receptors' expression. },

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid25873270,

title = {Effects of prenatal stress on anxiety-like behavior and nociceptive response in rats},

author = {N Said and S Lakehayli and O Battas and F Hakkou and A Tazi},

url = {https://pubmed.ncbi.nlm.nih.gov/25873270/},

doi = {10.1142/S0219635215500107},

issn = {0219-6352},

year  = {2015},

date = {2015-06-01},

urldate = {2015-06-01},

journal = {J Integr Neurosci},

volume = {14},

number = {2},

pages = {223--234},

abstract = {We assess the anxiety-like behavior in the open field and elevated plus maze tests and measure the nociceptive response in the tail flick test following prenatal stress exposure in adult male and female Wistar rats. In both behavioral anxiety tests, prenatal stress increased the anxiety-like behavior in male PS rats, but not in females suggesting a strong sex-dependent anxiogenic effect. The tail flick results showed a hypersensitivity to pain in male and female PS rats with a subtle gender difference. These findings suggest that prenatal stress is an important risk factor for multiple mental disorders. },

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid25896010,

title = {Effect of prenatal stress on memory, nicotine withdrawal and 5HT1A expression in raphe nuclei of adult rats},

author = {N Said and S Lakehayli and M El Khachibi and M El Ouahli and S Nadifi and F Hakkou and A Tazi},

doi = {10.1016/j.ijdevneu.2015.04.008},

issn = {1873-474X},

year  = {2015},

date = {2015-06-01},

urldate = {2015-06-01},

journal = {Int J Dev Neurosci},

volume = {43},

pages = {92--98},

abstract = {Maternal distress has often been associated with cognitive deficiencies and drug abuse in rats. This study examined these behavioral effects in offspring of mothers stressed during gestation. To this end, pregnant dams were subjected to daily electric foot shocks during the last 10 days of pregnancy. We measured litter parameters and body weights of the descendants after weaning (21 days) and at adulthood (80 days). Afterwards, prenatally stressed and control rats' performances in the novel object recognition test were compared in order to evaluate their memory while others underwent the Water consumption test to assess the nicotine withdrawal intensity after perinatal manipulations. Meanwhile, another set of rats were sacrificed and 5HT1A receptors' mRNA expression was measured in the raphe nuclei by quantitative Real Time PCR. We noticed no significant influence of maternal stress on litter size and body weight right after weaning. However, control rats were heavier than the stressed rats in adulthood. The results also showed a significant decrease in the recognition score in rats stressed in utero compared to the controls. Moreover, a heightened anxiety symptom was observed in the prenatally stressed offspring following nicotine withdrawal. Additionally, the Real Time PCR method revealed that prenatal stress induced a significant decrease in 5HT1A receptors' levels in the raphe nuclei. Nicotine had a similar effect on these receptors' expression in both nicotine-treated control and prenatally stressed groups. Taken together, these findings suggest that the cognitive functions and drug dependence can be triggered by early adverse events in rats. },

keywords = {},

pubstate = {published},

tppubtype = {article}

}