Life-long overexpression of S100β in Down’s syndrome: implications for Alzheimer pathogenesis

Griffin, W. Sue T.; Sheng, Jin; McKenzie, Jeanette E.; Royston, M.C.; Gentleman, Steve; Brumback, Roger A.; Cork, Linda C.; Bigio, Marc R. Del; Roberts, Gareth W.; Mrak, Robert E.

doi:10.1016/s0197-4580(98)00074-8

Cited by 125 publications

(72 citation statements)

References 20 publications

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“…In fact, it has been shown that S100B production is up-regulated in patients with AD (Mrak and Griffin, 2001), and overexpression of S100B precedes the appearance of neuritic ␤-amyloid plaque pathology in a transgenic mouse model of AD (Sheng et al, 2000). Moreover, neuritic changes in ␤-amyloid plaques in Down's syndrome were shown to be closely associated with astrocytic overproduction of S100B (Griffin et al, 1998a). Thus, the above findings may be interpreted as S100B being an important perpetrator in the progression of diffuse, nonfibrillar ␤-amyloid plaques to neuritic ␤-amyloid plaques, thereby exacerbating the progression of AD pathology (Mrak et al, 1996;Mrak and Griffin, 2001).…”

Section: Discussionmentioning

confidence: 99%

Arundic Acid Ameliorates Cerebral Amyloidosis and Gliosis in Alzheimer Transgenic Mice

Mori

Town²,

Tan³

et al. 2006

J Pharmacol Exp Ther

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Section: Discussionmentioning

confidence: 99%

Arundic Acid Ameliorates Cerebral Amyloidosis and Gliosis in Alzheimer Transgenic Mice

Mori

Town²,

Tan³

et al. 2006

J Pharmacol Exp Ther

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“…High concentrations of S100␤ results in a potent activation of inducible nitric oxide synthase (iNOS) and a subsequent generation of nitric oxide (NO), resulting in astrocytic cell death (37). In Alzheimers disease and in Downs syndrom where chronic glial activation occurs, S100 beta levels in several affected brain regions are elevated several-fold compared with age-matched controls (38). Children with Down syndrome regardless of age, have basal levels of S100 comparable to those in neonates (23).…”

Section: Discussionmentioning

confidence: 99%

“…Serum samples from cord blood (arterial and venous blood mixed) from a control group of 32 term newborn infants, gestational age, median (range) 40 (37)(38)(39)(40)(41)(42) weeks, were collected before the study started. The control infants, all with Apgar score Ն 9 at 1, 5 and 10 min, were born 1995-96 after uncomplicated vaginal delivery with a mean umbilical artery pH of 7.26 (SD 0.07) and a mean BD of 5 mmol/L (SD 2.7).…”

Section: Methodsmentioning

confidence: 99%

S100 Protein in Serum as a Prognostic Marker for Cerebral Injury in Term Newborn Infants with Hypoxic Ischemic Encephalopathy

et al. 2004

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The astroglial protein S100 is an established biochemical marker for CNS injury in the adult. The aim was to investigate whether S100 in serum is a prognostic marker of cerebral injury in term newborn infants with hypoxic ischemic encephalopathy (HIE) after perinatal asphyxia. Serum S100 was measured on postnatal days 1-4 in 62 term infants with birth asphyxia. The infants were classified for HIE and had follow-up for at least 18 mo. Infants with moderate and severe HIE had significantly higher S100 levels on postnatal day 1 (p ϭ 0.031) and day 2 (p ϭ 0.008) than infants with mild or no HIE. The levels of S100 decreased on days 2 and 3 in all infants with HIE. The median S100 level on postnatal day 1 was higher in nine infants who died neonatally and in 10 infants who developed cerebral palsy (CP), compared with 43 infants with no signs of impairment at follow up, 14.0 (0.5-60.0) g/L, 20.7 (0.2-64.0) g/L and 5.5 (0.7-120.0) g/L, respectively. A level of S100 above 12 g/L the first day of life was significantly more frequent in infants who died or developed CP than in infants with no impairment at follow up (p ϭ 0.02). Increased S100 levels were significantly inversely correlated with perinatal pH in the infants and associated with abnormal CTG at admission to the labor ward. Early determination of serum S100 may reflect the extent of brain damage in infants with HIE after asphyxia. Abbreviations CP, cerebral palsy CSF, cerebrospinal fluid CTG, cardiotocography FHR, fetal heart rate HIE, hypoxic ischemic encephalopathy S100, S100 protein including the subunits ␣␤ and ␤␤ aEEG, amplitude integrated EEG GFAP, glial fibrillary acidic protein Birth asphyxia remains a considerable problem in perinatal medicine with an incidence around 0.6 -0.8% of births (1-3). About half of these infants develop hypoxic ischemic encephalopathy (HIE) (2, 4). Those with moderate and severe HIE are at high risk of developing cerebral palsy (CP) (5-8). Prognostic assessment of brain injury after perinatal asphyxia will become essential for proper selection concerning early cerebroprotective treatment, which might be a likely option in the near future (9, 10). Several biochemical markers in cerebrospinal fluid (CSF) have been associated with cerebral complications in infants after perinatal asphyxia (11-14) and recently also S100 in CSF (15). A prognostic marker in serum would be of great value. S100 is a calcium binding protein present in the CNS. The dimers ␣␤ and ␤␤ of S100 are mainly specific for the nervous system and present chiefly in the astroglial cells of the CNS (16,17). S100 ␣␣ is present in many organs outside the CNS and will not be discussed in this report, where S100 will be used for the brain-specific S100 with subunits ␣␤ and ␤␤.The astroglial protein S100 is an established biochemical marker for CNS injury in the adult, in whom increased levels of S100 in CSF have been reported after cerebral insults (18,19). S100 in blood has been shown to be a marker of brain damage in adult stroke (20, 21) and a potential marker for c...

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“…␣7nAChR, ␣7-Nicotinic acetylcholine receptor; AMPAR, AMPA receptor. S100␤ and superoxide dismutase, have been implicated in amyloid deposition and metabolism, as has increased BACE1 (␤-site APPcleaving enzyme) maturation and activity (Griffin et al, 1998;Wolvetang et al, 2003;Lott et al, 2006). Several mouse models of DS have been established.…”

Section: ␤ Amyloid and Down Syndromementioning

confidence: 99%

β-Amyloid Modulation of Synaptic Transmission and Plasticity

Venkitaramani¹,

Chin²,

Netzer³

et al. 2007

J. Neurosci.

105

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Life-long overexpression of S100β in Down’s syndrome: implications for Alzheimer pathogenesis

Cited by 125 publications

References 20 publications

Arundic Acid Ameliorates Cerebral Amyloidosis and Gliosis in Alzheimer Transgenic Mice

Arundic Acid Ameliorates Cerebral Amyloidosis and Gliosis in Alzheimer Transgenic Mice

S100 Protein in Serum as a Prognostic Marker for Cerebral Injury in Term Newborn Infants with Hypoxic Ischemic Encephalopathy

β-Amyloid Modulation of Synaptic Transmission and Plasticity

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