Neuron loss in APP transgenic mice

Calhoun, Michael E.; Wiederhold, Karl‐Heinz; Abramowski, Dorothée; Phinney, Amie L.; Probst, A.; Stürchler-Pierrat, Christine; Staufenbiel, Matthias; Sommer, Bernd; Jucker, Mathias

doi:10.1038/27351

Cited by 452 publications

(278 citation statements)

References 7 publications

Supporting

Mentioning

251

Contrasting

Unclassified

Order By: Relevance

“…A substantial but comparable variability in plaque load was seen within the two groups of mice (Figure 3), consistent with observations at early stages of plaque formation in other lines of hAPP ϩ/Ϫ SR ϩ/ϩ mice. 5,7,27 The regional distribution and size of thioflavin S-stained plaques were also very similar in hAPP ϩ/Ϫ mice with or without SR expression (Figures 2 and 4). The plaque load was greatest in the hippocampus, and most callosal and neocortical plaques were found immediately overlying the hippocampus.…”

Section: Lack Of the Sr Does Not Affect Amyloid Plaque Deposition In mentioning

confidence: 71%

Elimination of the Class A Scavenger Receptor Does Not Affect Amyloid Plaque Formation or Neurodegeneration in Transgenic Mice Expressing Human Amyloid Protein Precursors

Huang

Buttini

Wyss‐Coray

et al. 1999

The American Journal of Pathology

View full text Add to dashboard Cite

Section: Lack Of the Sr Does Not Affect Amyloid Plaque Deposition In mentioning

confidence: 71%

Elimination of the Class A Scavenger Receptor Does Not Affect Amyloid Plaque Formation or Neurodegeneration in Transgenic Mice Expressing Human Amyloid Protein Precursors

Huang

Buttini

Wyss‐Coray

et al. 1999

The American Journal of Pathology

View full text Add to dashboard Cite

“…Indeed, this may explain, at least in part, why the many available murine models of AD fail to fully reproduce the pathologic changes of AD in humans. Besides the absence of neurofibrillary changes, most of these animal models do not demonstrate overt neuronal loss (Irizarry et al, 1997a, b ), with some exceptions (Calhoun et al, 1998). Several explanations have been proposed for this phenomenon including species variability in neuronal vulnerability, lack of certain human-type inflammatory factors and tau protein (Hardy and Selkoe, 2002), as well as species variability in Aβ burden and different types of plaques that accumulate in different tg mouse models (Bondolfi et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Amyloid precursor protein increases cortical neuron size in transgenic mice

Savonenko

King

et al. 2009

Neurobiology of Aging

View full text Add to dashboard Cite

The amyloid precursor protein (APP) is the source of β-amyloid, a pivotal peptide in the pathogenesis of Alzheimer's disease (AD). This study examines the possible effect of APP transgene expression on neuronal size by measuring the volumes of cortical neurons (μm 3 ) in transgenic mouse models with familial AD Swedish mutation (APPswe), with or without mutated presenilin1 (PS1dE9), as well as in mice carrying wild-type APP (APPwt). Overexpression of APPswe and APPwt protein, but not of PS1dE9 alone, resulted in a greater percentage of medium-sized neurons and a proportionate decrease in the percentage of small-sized neurons. Our observations indicate that the overexpression of mutant (APPswe) or wild-type APP in transgenic mice is necessary and sufficient for hypertrophy of cortical neurons. This is highly suggestive of a neurotrophic effect and also raises the possibility that the lack of neuronal loss in transgenic mouse models of AD may be attributed to overexpression of APP.

show abstract

“…The congophilic, densecore Ab deposits show many characteristics of human AD plaques such as enlarged dystrophic neurites [29]. Similar to AD, vascular amyloid is also present in aged APP23 animals [30].…”

Section: Animal Models Of Alzheimer's Diseasementioning

confidence: 97%

Estrogen anti-inflammatory activity in brain: A therapeutic opportunity for menopause and neurodegenerative diseases

Vegeto

Benedusi

Maggi

2008

Frontiers in Neuroendocrinology

262

202

View full text Add to dashboard Cite

a b s t r a c tRecent studies highlight the prominent role played by estrogens in protecting the central nervous system (CNS) against the noxious consequences of a chronic inflammatory reaction. The neurodegenerative process of several CNS diseases, including Multiple Sclerosis, Alzheimer's and Parkinson's Diseases, is associated with the activation of microglia cells, which drive the resident inflammatory response. Chronically stimulated during neurodegeneration, microglia cells are thought to provide detrimental effects on surrounding neurons. The inhibitory activity of estrogens on neuroinflammation and specifically on microglia might thus be considered as a beneficial therapeutic opportunity for delaying the onset or progression of neurodegenerative diseases; in addition, understanding the peculiar activity of this female hormone on inflammatory signalling pathways will possibly lead to the development of selected anti-inflammatory molecules. This review summarises the evidence for the involvement of microglia in neuroinflammation and the anti-inflammatory activity played by estrogens specifically in microglia.

show abstract

Neuron loss in APP transgenic mice

Cited by 452 publications

References 7 publications

Elimination of the Class A Scavenger Receptor Does Not Affect Amyloid Plaque Formation or Neurodegeneration in Transgenic Mice Expressing Human Amyloid Protein Precursors

Elimination of the Class A Scavenger Receptor Does Not Affect Amyloid Plaque Formation or Neurodegeneration in Transgenic Mice Expressing Human Amyloid Protein Precursors

Amyloid precursor protein increases cortical neuron size in transgenic mice

Estrogen anti-inflammatory activity in brain: A therapeutic opportunity for menopause and neurodegenerative diseases

Contact Info

Product

Resources

About