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Home › Research › Topics › samp8

samp8

5 studies tagged samp8, dated 2001-01-01 to 2016-10-01. Bibliography: BibTeX (.bib) · RIS (.ris)

Newest in this topic

  1. Peripheral Administration of GSK-3β Antisense Oligonucleotide Improves Learning and Memory in SAMP8 and Tg2576 Mouse Models of Alzheimer's Disease 2016-10-01
  2. Antisense directed against PS-1 gene decreases brain oxidative markers in aged senescence accelerated mice (SAMP8) and reverses learning and memory impairment: a proteomics study 2013-06-15
  3. Peripheral administration of antisense oligonucleotides targeting the amyloid-β protein precursor reverses AβPP and LRP-1 overexpression in the aged SAMP8 mouse brain 2012-01-01

Studies

5 studies carry this tag.

Date range

2001 to 2016

Top journals

  • Journal of Alzheimer's disease : JAD 2
  • Biochemistry and cell biology = Biochimie et biologie cellulaire 1
  • Experimental neurology 1
  • Free radical biology & medicine 1

Newest first, then by address. Each study has a usefulness score out of 100 (rubric version 4.0); tap a score to see what makes it up. Tags were assigned automatically from each study's title and summary. The same studies as a filter in the library.

  1. Peripheral Administration of GSK-3β Antisense Oligonucleotide Improves Learning and Memory in SAMP8 and Tg2576 Mouse Models of Alzheimer's Disease

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Journal of Alzheimer's disease : JAD 2016-10-01 Drug development

    Glycogen synthase kinase (GSK)-3β is a multifunctional protein that has been implicated in the pathological characteristics of Alzheimer's disease (AD), including the heightened levels of neurofibrillary tangles, amyloid-beta (Aβ), and neurodegeneration.

  2. Antisense directed against PS-1 gene decreases brain oxidative markers in aged senescence accelerated mice (SAMP8) and reverses learning and memory impairment: a proteomics study

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Free radical biology & medicine 2013-06-15 Drug development

    Amyloid β-peptide (Aβ) plays a central role in the pathophysiology of Alzheimer's disease (AD) through the induction of oxidative stress.

  3. Peripheral administration of antisense oligonucleotides targeting the amyloid-β protein precursor reverses AβPP and LRP-1 overexpression in the aged SAMP8 mouse brain

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Journal of Alzheimer's disease : JAD 2012-01-01 Drug development

    The senescence accelerated mouse-prone 8 (SAMP8) mouse model of Alzheimer's disease has a natural mutation leading to age-related increases in the amyloid-β protein precursor (AβPP) and amyloid-β (Aβ) in the brain, memory impairment, and deficits in Aβ removal from the brain.

  4. Anti-amyloid beta protein antibody passage across the blood-brain barrier in the SAMP8 mouse model of Alzheimer's disease: an age-related selective uptake with reversal of learning impairment

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Experimental neurology 2007-05-22 Treatments

    Amyloid beta protein (Abeta) levels are elevated in the brain of Alzheimer's disease patients.

  5. Molecular cloning, expression, and regulation of hippocampal amyloid precursor protein of senescence accelerated mouse (SAMP8)

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Biochemistry and cell biology = Biochimie et biologie cellulaire 2001-01-01 Drug development

    Alzheimer's disease (AD) is associated with increased expression of amyloid precursor protein (APP) with a consequent deposition of amyloid beta peptide (Abeta) which forms characteristic senile plaques.

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