gliosis/nikótín

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Neonatal Nicotine Exposure Leads to Hypothalamic Gliosis in Adult Overweight Rats.

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Astrocytes and microglia, the immune competent cells of central nercous system, can be activated in response to metabolic signals such as obesity and hyperleptinaemia. In rats, maternal exposure to nicotine during lactation leads to central obesity, hyperleptinaemia, leptin resistance and

Hypothalamic Neuropeptides Expression and Hypothalamic Inflammation in Adult Rats that Were Exposed to Tobacco Smoke during Breastfeeding: Sex-Related Differences.

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The hypothalamus controls food intake and energy expenditure. In rats, maternal exposure to nicotine during breastfeeding alters the hypothalamic circuitry of the adult offspring, resulting in leptin resistance, neuropeptides changes and gliosis. Tobacco smoke exposure during lactation causes

Neuropathology of the area postrema in sudden intrauterine and infant death syndromes related to tobacco smoke exposure.

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The area postrema is a densely vascularized small protuberance at the inferoposterior limit of the fourth ventricle, outside of the blood-brain barrier. This structure, besides to induce emetic reflex in the presence of noxious chemical stimulation, has a multifunctional integrative capacity to send

Effects of prenatal cigarette smoke exposure on BDNF, PACAP, microglia and gliosis expression in the young male mouse brainstem.

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Cigarette smoke exposure during pregnancy into infancy affects brain growth and development in both short and long term (into adulthood). Using a mouse model of pre- into post- natal cigarette smoke exposure (SE), we aimed to determine the effects on brain derived neurotrophic factor (BDNF) and its

Long-lasting CNS effects of a short-term chemical knockout of ornithine decarboxylase during development: nicotinic cholinergic receptor upregulation and subtle macromolecular changes in adulthood.

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Ornithine decarboxylase (ODC) and the polyamines play an essential role in brain cell replication and differentiation and polyamines also regulate the function of nicotinic acetylcholine receptors (nAChRs). We administered alpha-difluoromethylornithine (DFMO), an irreversible inhibitor of ODC, to

Alpha7 nicotinic acetylcholine receptor expression in Alzheimer's disease: receptor densities in brain regions of the APP(SWE) mouse model and in human peripheral blood lymphocytes.

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The brains of people with Alzheimer's disease (AD) display several characteristic pathological features, including deposits (plaques) of beta-amyloid 1-42 (Abeta1-42), intraneuronal accumulations (tangles) of hyperphosphorylated tau, degeneration of the basal forebrain cholinergic pathway, and

Neurobehavioral management of behavioral anomalies in frontal lobe syndrome.

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Neurobehavioral approach uses behavioral paradigm towards comprehensive rehabilitation by identifying the neurological or neuropsychological constraints that can interfere with learning and behavior of an individual. The present case study highlights the role of functional skills approach in

Possible pathomechanisms of sudden infant death syndrome: key role of chronic hypoxia, infection/inflammation states, cytokine irregularities, and metabolic trauma in genetically predisposed infants.

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Chronic hypoxia, viral infections/bacterial toxins, inflammation states, biochemical disorders, and genetic abnormalities are the most likely trigger of sudden infant death syndrome (SIDS). Autopsy studies have shown increased pulmonary density of macrophages and markedly more eosinophils in the

Positive modulators of the α7 nicotinic receptor against neuroinflammation and cognitive impairment in Alzheimer's disease.

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Evidence so far indicates that therapies targeting a single aspect of Alzheimer's disease (AD) have no sufficient efficacy in diminishing long-term the progression of AD. Neuroinflammation is an early event during the development of the disease and it is thought to exacerbate the abnormal

³H-deprenyl and ³H-PIB autoradiography show different laminar distributions of astroglia and fibrillar β-amyloid in Alzheimer brain.

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BACKGROUND The pathological features in Alzheimer's disease (AD) brain include the accumulation and deposition of β-amyloid (Aβ), activation of astrocytes and microglia and disruption of cholinergic neurotransmission. Since the topographical characteristics of these different pathological processes

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