Definition of Genes and Paths Involved in Alzheimers Disease: Using Gene Expression Profiles and Chemical Genetics at the Mouse Brain Level

Wu, Pu; Hu, Yinghe

doi:10.2174/138920206778604368

Cited by 4 publications

(2 citation statements)

References 86 publications

(124 reference statements)

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“…DNA microarray technology is a useful tool to dissect the mechanism underlying brain dysfunction and ageing (Wu & Hu, 2006). To understand the molecular basis of neurodegenerative phenotypes, we have analysed the gene expression profiles in the brains of 3-and 10-month-old cDKO mice.…”

Section: Discussionmentioning

confidence: 99%

Environment enrichment rescues the neurodegenerative phenotypes in presenilins‐deficient mice

Shen

et al. 2007

Eur J of Neuroscience

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Presenilin (PS) 1 and 2 conditional double knockout (cDKO) mice show progressive memory dysfunction and forebrain degeneration. Gene expression profiling results revealed a strong activation of immunity and inflammation responses in the brains of 10-month-old cDKO mice. As environmental enrichment (EE) has been shown to be able to improve memory and induce neurogenesis of the brain, we assessed the effects of EE on the memory performance and the neurodegeneration in cDKO mice. We found that EE effectively enhanced memory and partially rescued the forebrain atrophy of the cDKO mice. Our results suggest that immunity and inflammation could play important roles in the neurodegeneration of cDKO mice. Furthermore, the beneficial effects of EE may be associated with the inhibition of the expression of immunity and inflammation-related genes in the brain.

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Section: Discussionmentioning

confidence: 99%

Environment enrichment rescues the neurodegenerative phenotypes in presenilins‐deficient mice

Shen

et al. 2007

Eur J of Neuroscience

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“…Different studies have demonstrated the essential role of the APOE gene (with the APOE4 allele increasing risk and the APOE2allele decreasing risk) both in familial late-onset and sporadic AD patients [12-15]. Different efforts have been made to identify others genetic factors involved in the pathophysiology of LOAD [16]. Association studies for specific candidate genes, selected because of their known biological function relevant to AD, have been performed for over 350 single nucleotide polymorphisms (SNP) of different genes including interleukin 1A (IL-1A), interleukin 1B (IL-1B), interleukin 1 receptor antagonist (IL-1RN) [17, 18], and methylentetrahydrofolate reductase (MTHFR) [19, 20].…”

Section: Introductionmentioning

confidence: 99%

Role of the Transforming-Growth-Factor-β1 Gene in Late-Onset Alzheimer’s Disease: Implications for the Treatment

Bosco

Ferri²,

Salluzzo³

et al. 2013

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Late-onset Alzheimer's disease (LOAD) is the most common form of dementia in the elderly. LOAD has a complex and largely unknown etiology with strong genetic determinants. Genetics of LOAD is known to involve several genetic risk factors among which the Apolipoprotein E (APOE) gene seems to be the major recognized genetic determinant. Recent efforts have been made to identify other genetic factors involved in the pathophysiology of LOAD such as genes associated with a deficit of neurotrophic factors in the AD brain. Genetic variations of neurotrophic factors, such as brain-derived neurotrophic factor (BDNF), and transforming-growth-factor-β1 (TGF-β1) are known to increase the risk to develop LOAD and have also been related to depression susceptibility in LOAD. Transforming-Growth-Factor-β1 (TGF-β1) is a neurotrophic factor that exerts neuroprotective effects against ß-amyloid-induced neurodegeneration. Recent evidence suggests that a specific impairment in the signaling of TGF-β is an early event in the pathogenesis of AD. TGF-β1 protein levels are predominantly under genetic control, and the TGF-β1 gene, located on chromosome 19q13.1–3, con-tains several single nucleotide polymorphisms (SNPs) upstream and in the transcript region, such as the SNP at codon +10 (T/C) and +25 (G/C), which is known to influence the level of expression of TGF-β1. In the present review, we summarize the current literature on genetic risk factors for LOAD, focusing on the role of the TGF-β1 gene, finally discussing the possible implications of these genetic studies for the selection of patients eligible for neuroprotective strategies in AD.

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Systematic gene expression profile of hypothalamus in calorie-restricted mice implicates the involvement of mTOR signaling in neuroprotective activity

Jiang

Shen

et al. 2009

Mechanisms of Ageing and Development

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Definition of Genes and Paths Involved in Alzheimers Disease: Using Gene Expression Profiles and Chemical Genetics at the Mouse Brain Level

Cited by 4 publications

References 86 publications

Environment enrichment rescues the neurodegenerative phenotypes in presenilins‐deficient mice

Environment enrichment rescues the neurodegenerative phenotypes in presenilins‐deficient mice

Role of the Transforming-Growth-Factor-β1 Gene in Late-Onset Alzheimer’s Disease: Implications for the Treatment

Systematic gene expression profile of hypothalamus in calorie-restricted mice implicates the involvement of mTOR signaling in neuroprotective activity

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