Intraneuronal amyloid precursor protein (APP) and appearance of extracellular β‐amyloid peptide (aβ) in the brain of aging kokanee salmon

Maldonado, Tammy A.; Jones, Richard E.; Norris, David O.

doi:10.1002/neu.10086

Cited by 22 publications

(22 citation statements)

References 78 publications

(96 reference statements)

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“…. White dot at base of a "percent pyknotic" bar means that the initial A␤ deposition appeared at that stage (from Maldonado et al, 2002). No A␤ deposition occurred in the Dp.…”

Section: Neurodegeneration In the Entire Salmon Brainmentioning

confidence: 96%

“…Maldonado et al (2000b) reported that brains of spawning but not immature kokanee salmon exhibit extracellular deposits of ␤-amyloid (A␤) peptide as well as senile A␤-plaques similar to those described in aging humans. Furthermore, the amount of A␤ increased with reproductive stage (Maldonado et al, 2002). However, it is not clear if neurodegeneration is positively correlated with this amyloidosis in the senescent salmon brain.…”

Section: Introductionmentioning

confidence: 94%

“…These regions included those that exhib-ited A␤ 1-42 and APP immunoreactivity in mature or spawning fish, as well as several control regions that in previous studies never exhibited A␤ immunoreactivity (Maldonado et al, 2000b(Maldonado et al, , 2002. Sections were examined by microscopic analysis, and salmon brain regions were identified using the atlas in Maldonado et al (2000b) and other maps of the kokanee salmon brain (Satou et al, 1984;and Shiga et al, 1985).…”

Section: Neuroanatomical Localizationmentioning

confidence: 99%

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Timing of neurodegeneration and beta‐amyloid (Aβ) peptide deposition in the brain of aging kokanee salmon

2002

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Brains of kokanee salmon (Oncorhynchus nerka kennerlyi) in one of four reproductive stages (sexually immature, maturing, sexually mature, and spawning) were stained with cresyl violet and silver stain to visualize neurodegeneration. These reproductive stages correlate with increasing somatic aging of kokanee salmon, which die after spawning. Twenty-four regions of each brain were examined. Brains of sexually immature fish exhibited low levels of neurodegeneration, whereas neurodegeneration was more marked in maturing fish and greatest in spawning fish. Neurodegeneration was present in specific regions of the telencephalon, diencephalon, mesencephalon, and rhombencephalon. Pyknotic neurons were observed in all regions previously reported to be immunopositive for A beta. Regions that did not exhibit neurodegeneration during aging included the magnocellular vestibular nucleus, the nucleus lateralis tuberis of the hypothalamus, and Purkinje cells of the cerebellum, all of which also lack A beta; perhaps these regions are neuroprotected. In 14 of 16 brain areas for which data were available on both the increase in A beta deposition and pyknosis, neurodegeneration preceded or appeared more or less simultaneously with A beta production, whereas in only two regions did A beta deposition precede neurodegeneration. This information supports the hypothesis that A beta deposition is a downstream product of neurodegeneration in most brain regions. Other conclusions are that the degree of neurodegeneration varies among brain regions, neurodegeneration begins in maturing fish and peaks in spawning fish, the timing of neurodegeneration varies among brain regions, and some regions do not exhibit accelerated neurodegeneration during aging.

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“…. White dot at base of a "percent pyknotic" bar means that the initial A␤ deposition appeared at that stage (from Maldonado et al, 2002). No A␤ deposition occurred in the Dp.…”

Section: Neurodegeneration In the Entire Salmon Brainmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 94%

Section: Neuroanatomical Localizationmentioning

confidence: 99%

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Timing of neurodegeneration and beta‐amyloid (Aβ) peptide deposition in the brain of aging kokanee salmon

2002

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“…For example, elevations in post-reproductive LH may drive neurological and vascular diseases while The large dyotic signaling in salmon (and other semelparous species) post-reproduction leads to dramatic and rapid (within 1-3 weeks) changes in tissue structure and function (phenoptosis) that are similar to the degenerative changes found in other aging vertebrates, including humans: the brain (amyloidosis), liver, stomach (peptic ulcers), spleen, thymus, thyroid, pituitary, kidney, and cardiovascular system exhibit degenerative changes, the adrenocortical tissue and pancreas display hyperplasia, and immune system collapse results in skin infections (Dickhoff et al 1989;Maldonado et al 2000Maldonado et al , 2002aWexler 1960, 1962). At this time, the suppression by 17β-estradiol on the utilization of pregnenolone as a substrate for cortisol synthesis by the interrenals (adrenals) is lost (McQuillan et al 2003).…”

Section: Ratio Of Sex Steroid/gonadotropin As a Measure Of Dyotic Sigmentioning

confidence: 96%

Does the degree of endocrine dyscrasia post-reproduction dictate post-reproductive lifespan? Lessons from semelparous and iteroparous species

et al. 2017

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Post-reproductive lifespan varies greatly among species; human post-reproductive lifespan comprises~30-50% of their total longevity, while semelparous salmon and dasyurid marsupials post-reproductive lifespan comprises <4% of their total longevity. To examine if the magnitude of hypothalamic-pituitarygonadal (HPG) axis dyscrasia at the time of reproductive senescence determines post-reproductive lifespan, we examined the difference between pre-and postreproductive (1) circulating sex hormones and (2) the ratio of sex steroids to gonadotropins (e.g., 17β-estradiol/follicle-stimulating hormone (FSH)), an index of the dysregulation of the HPG axis and the level of dyotic (death) signaling post-reproduction. Animals with a shorter post-reproductive lifespan (<4% total longevity) had a more marked decline in circulating sex steroids and corresponding elevation in gonadotropins compared to animals with a longer post-reproductive lifespan (30-60% total longevity). In semelparous female salmon of short post-reproductive lifespan (1%), these divergent changes in circulating hormone concentration postreproduction equated to a 711-fold decrease in the ratio of 17β-estradiol/FSH between the reproductive and post-reproductive periods. In contrast, the decrease in the ratio of 17β-estradiol/FSH in iteroparous female mammals with long post-reproductive lifespan was significantly less (1.7-34-fold) post-reproduction. Likewise, in male semelparous salmon, the decrease in the ratio of testosterone/FSH (82-fold) was considerably larger than for iteroparous species (1.3-11-fold). These results suggest that (1) organisms with greater reproductive endocrine dyscrasia more rapidly undergo senescence and die, and (2) the contribution postreproduction by non-gonadal (and perhaps gonadal) tissues to circulating sex hormones dictates postreproductive tissue health and longevity. In this way, reproduction and longevity are coupled, with the degree of non-gonadal tissue hormone production dictating the rate of somatic tissue demise post-reproduction and the differences in post-reproductive lifespans between species.

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“…SAA is highly conserved between fish and humans (Lashuel, 2008), and aging Pacific salmon undergo a rapid senescence with accompanying A amyloid build-up in their brains (Maldonado, Jones and Norris, 2002), but apparently only one report of systemic amyloidosis in fish appears in the literature and the muscles did not seem affected (Mashima, Cornish and Lewbart, 1997). Liver involvement raised the possibility that a product such as cod liver oil could potentially be contaminated, but protein fractions should largely be purified out of fish oil preparations.…”

Section: Other Dietary Sources Of Amyloid Fibrilsmentioning

confidence: 99%

Amyloid fibrils: potential food safety implications

Greger

2008

IJFSNPH

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Abstract:The demonstration of oral Amyloid-A (AA) fibril transmissibility has raised food safety questions about the consumption of amyloidotic viscera. In a presumed prion-like mechanism, amyloid fibrils have been shown to trigger and accelerate the development of AA amyloidosis in rodent models. The finding of amyloid fibrils in edible avian and mammalian food animal tissues, combined with the inability of cooking temperatures to eliminate their amyloidogenic potential, has led to concerns that products such as pâté de foie gras may activate a reactive systemic amyloidosis in susceptible consumers. Given the ability of amyloid fibrils to cross-seed the formation of chemically heterologous fibrils, the speculative etiologic role of dietary amyloid in other disease processes involving amyloid formation such as Alzheimer's disease and Type II Diabetes is also discussed.

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Intraneuronal amyloid precursor protein (APP) and appearance of extracellular β‐amyloid peptide (aβ) in the brain of aging kokanee salmon

Cited by 22 publications

References 78 publications

Timing of neurodegeneration and beta‐amyloid (Aβ) peptide deposition in the brain of aging kokanee salmon

Timing of neurodegeneration and beta‐amyloid (Aβ) peptide deposition in the brain of aging kokanee salmon

Does the degree of endocrine dyscrasia post-reproduction dictate post-reproductive lifespan? Lessons from semelparous and iteroparous species

Amyloid fibrils: potential food safety implications

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