Early Amyloid Accumulation in the Hippocampus of SAMP8 Mice

Valle, Jaume del; Duran-Vilaregut, Joaquim; Manich, Gemma; Casadesús, Gemma; Smith, Mark A.; Camins, Antoni; Pallàs, Mercè; Pelegrí, Carme; Vilaplana, Jordi

doi:10.3233/jad-2010-1321

Cited by 117 publications

(109 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The deposits described have included, among others, β/A4 protein-like immunoreactivity granular structures (β-LIGS) (Takemura et al 1993), amyloid β-peptide-like immunoreactivity deposits (Aβ-LI) (Fukunari et al 1994), reelin deposits that contained Aβ (Knuesel et al 2009) and the hippocampal granules containing Aβ(1-40) and Aβ(1-42) (Del Valle et al 2010;Currais et al 2012;Porquet et al 2013;Yamaguchi et al 2012). Morley et al (2000) found Aβ plaques that were not discernible before 16 months of age and became more prevalent at 22 months of age.…”

Section: Discussionmentioning

confidence: 99%

“…One such change is the appearance of clustered pathological granular structures that are mainly located in the hippocampus. These clustered granules have been extensively described in the brain of several strains of aged mice, including C57BL/6 (Lamar et al 1976;Jucker et al 1994;Soontornniyomkij et al 2012), ICR-CD1 (Del Valle et al 2010), AKR (Mitsuno et al 1999) and senescence-accelerated mouse prone mouse 8 (SAMP8; Akiyama et al 1986;Kuo et al 1996;Del Valle et al 2010). In all strains, these granules start their development in the stratum radiatum of CA1, and thereafter, the number of clusters increases and they spreadin size, are clustered in groups of 40-50 (Akiyama et al 1986;Del Valle et al 2010;Kuo et al 1996).…”

Section: Introductionmentioning

confidence: 93%

“…Several studies have described an increase in both amyloid β precursor protein (AβPP) and derived β-amyloid (Aβ) peptides in the brain of SAMP8 mice, as well as the presence of Aβ plaques or deposits Morley et al 2000;Takemura et al 1993). The presence of Aβ has also been described in the granular structures of the hippocampus (Del Valle et al 2010;Fukunari et al 1994;Currais et al 2012;Porquet et al 2013;Yamaguchi et al 2012). Furthermore, increased levels of hyperphosphorylated tau protein and tau deposits have also been described (Canudas et al 2005;Manich et al 2011;Wei et al 1999).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Presence of a neo-epitope and absence of amyloid beta and tau protein in degenerative hippocampal granules of aged mice

Manich

Valle

Cabezón

et al. 2013

AGE

Self Cite

View full text Add to dashboard Cite

Clustered pathological granules related to a degenerative process appear and increase progressively with age in the hippocampus of numerous mouse strains. We describe herein the presence of a neoepitope of carbohydrate nature in these granules, which is not present in other brain areas and thus constitutes a new marker of these degenerative structures. We also found that this epitope is recognised by a contaminant IgM present in several antibodies obtained from mouse ascites and from both mouse and rabbit sera. These findings entail the need to revise the high number of components that are thought to be present in the granules, such as the controversial β-amyloid peptides described in the granules of senescence-accelerated mouse prone-8 (SAMP8) mice. Characterisation of the composition of SAMP8 granules, taking into account the presence of the neo-epitope and the contaminant IgM, showed that granules do not contain either β-amyloid peptides or tau protein. The presence of the neo-epitope in the granules but not in other brain areas opens up a new direction in the study of the neurodegenerative processes associated with age. The SAMP8 strain, in which the progression of the granules is enhanced, may be a useful model for this purpose.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 93%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Presence of a neo-epitope and absence of amyloid beta and tau protein in degenerative hippocampal granules of aged mice

Manich

Valle

Cabezón

et al. 2013

AGE

Self Cite

View full text Add to dashboard Cite

show abstract

“…Furthermore, SAMP8 has been considered to be a sound model for investigating the pathophysiology of the early events in AD, due to Aβ accumulation [69,70], cerebral amyloid angiopathy [71], brain blood barrier alterations [71][72][73], and different hippocampal protein aggregates [74].…”

Section: Histopathological Similarities In Samp8 and Admentioning

confidence: 99%

Senescence-Accelerated Mice P8: A Tool to Study Brain Aging and Alzheimer's Disease in a Mouse Model

Pallàs

2012

ISRN Cell Biology

Self Cite

View full text Add to dashboard Cite

The causes of aging remain unknown, but they are probably intimately linked to a multifactorial process that affects cell networks to varying degrees. Although a growing number of aging and Alzheimer's disease (AD) animal models are available, a more comprehensive and physiological mouse model is required. In this context, the senescence-accelerated mouse prone 8 (SAMP8) has a number of advantages, since its rapid physiological senescence means that it has about half the normal lifespan of a rodent. In addition, according to data gathered over the last five years, some of its behavioral traits and histopathology resemble AD human dementia. SAMP8 has remarkable pathological similarities to AD and may prove to be an excellent model for acquiring more in-depth knowledge of the age-related neurodegenerative processes behind brain senescence and AD in particular. We review these facts and particularly the data on parameters related to neurodegeneration. SAMP8 also shows signs of aging in the immune, vascular, and metabolic systems, among others.

show abstract

“…25 Only one widely accepted spontaneous model of sporadic form of AD exists: senescence-accelerated SAMP mice. 3,22,26 This review is focused on our recent results, which offer promising evidence that the mechanisms of brain aging and neurodegenerative processes in senescence-accelerated OXYS rats are similar to those in AD. The OXYS rat strain was developed at the Institute of Cytology and Genetics, Russian Academy of Sciences (Novosibirsk), from Wistar stock via selection for susceptibility to cataractogenic effect of a galactose-rich diet and via inbreeding of highly susceptible rats.…”

Section: Introductionmentioning

confidence: 99%

Senescence-accelerated OXYS rats: A model of age-related cognitive decline with relevance to abnormalities in Alzheimer disease

et al. 2014

View full text Add to dashboard Cite

Senescence-accelerated OXYS rats are an experimental model of accelerated aging that was established from wistar stock via selection for susceptibility to cataractogenic effects of a galactose-rich diet and via subsequent inbreeding of highly susceptible rats. Currently, we have the 102nd generation of OXYS rats with spontaneously developing cataract and accelerated senescence syndrome, which means early development of a phenotype similar to human geriatric disorders, including accelerated brain aging. in recent years, our group found strong evidence that OXYS rats are a promising model for studies of the mechanisms of brain aging and neurodegenerative processes similar to those seen in Alzheimer disease (AD). The manifestation of behavioral alterations and learning and memory deficits develop since the fourth week of age, i.e., simultaneously with first signs of neurodegeneration detectable on magnetic resonance imaging and under a light microscope. in addition, impaired long-term potentiation has been demonstrated in OXYS rats by the age of 3 months. with age, neurodegenerative changes in the brain of OXYS rats become amplified. we have shown that this deterioration happens against the background of overproduction of amyloid precursor protein (AβPP), accumulation of β-amyloid (Aβ), and hyperphosphorylation of the tau protein in the hippocampus and cortex. The development of AMDlike retinopathy in OXYS rats is also accompanied by increased accumulation of Aβ in the retina. These published data suggest that the OXYS strain may serve as a spontaneous rat model of AD-like pathology and could help to decipher the pathogenesis of AD.

show abstract

Early Amyloid Accumulation in the Hippocampus of SAMP8 Mice

Cited by 117 publications

References 0 publications

Presence of a neo-epitope and absence of amyloid beta and tau protein in degenerative hippocampal granules of aged mice

Presence of a neo-epitope and absence of amyloid beta and tau protein in degenerative hippocampal granules of aged mice

Senescence-Accelerated Mice P8: A Tool to Study Brain Aging and Alzheimer's Disease in a Mouse Model

Senescence-accelerated OXYS rats: A model of age-related cognitive decline with relevance to abnormalities in Alzheimer disease

Contact Info

Product

Resources

About