Summary: Description of effects of many substances on various diseases on mice that age fast.
Paper by Masanory Hosokawa, Makiko Umezawa, Keiichi Higuchi and Toshio Takeda in Journal of Anti-Aging Medicine, Volume 1, Number 1, 1998.
(((bias: I don't pay much attention to mice as models of aging. I pay even less attention to accelerated-aging mice as models of aging. They seem too far removed. I also know squat about the subject)))
Most of the paper describes the Senescence accelerated mouse prone and resistant (SAMP and SAMR) variety of mice developed since the late 60s. They are closely related, and are both relatively normal until they reach maturity (((don't know when that is, but they become fertile at around 45 days))). After maturity, SAMR continues a relatively normal mouse life, but SAMP deteriorates rapidly in many different ways. Median life-span of SAMR mice is about the same as normal long-lived mice, although not the ones in their lab, which lived for around 19 months. Median life-span for SAMP mice varied between about 7 and 14 months depending on the sub-variety. They also use a degree-of-senescence score that is just how fucked they think the mouse is, and note a factor of 1.5-3.5 greater degree of senescence in SAMP mice over SAMR at 8 months of age. SAM mice, both varieties, tend to die from contracted kidneys, abscess formation (((balls of pus!?))), pneumonia and lymphomas (((not similar to the profile in humans))). The idea is that the SAMP is just an accelerated decline version of the SAMR.
It then describes a few sub-variants of the SAMP mice that are specially prone to osteoperosis, learning and memory problems, amyloidosis (((insoluble protein clumps in various organs))) and immune system decline.
It finishes with things they tried that helped with each one of those. Caloric restriction helped with the lifespan and the amyloidosis of SAMP mice (no measurement numbers given) (((Most interesting for me is that it didn't extend the SAMR lifespan))). Summary of the rest of the benefits found is as follows (no numbers are given for any of these):
Soy bean protein instead of casein for amyloidosis, aged garlic extract helped survival ratio of the sub-variety with problems with memory and immune-system (SAMP8). Toki-Shakuyaku-San (TSS) and Boui-Jiou-Tou (BJT) extended median survival of the amyloidosis prone mice (SAMP1). Deer antler (((!?!))) orally increased testosterone, decreased malondialdehyde (((a oxidative stress marker))) in the liver and brain, increased RNA and protein in the liver, increased liver super-oxide simutase, decreased monoamine oxidase B in liver and brain in SAMP8 males. Alpha-phenyl N-tertiary-butyl nitrone (PBN, a spin-trapping agent) (((free-radical capture))) increased lifespan of SAMP8. Acidic fibroblast growth factor (aFGF) protected the impairment of delayed type hypersensitivity reaction in SAMP8.
The osteoperosis-prone variety (SAMP6) was helped by mixing its bone marrow with those of another sub-variety, or getting bone marrow-derived factors from that other sub-variety, or by giving it calcium, parathyroid hormone or estrogen.
(((I'll skip the substances that helped memory and learning since I consider them even less relevant to humans than the others, but there's a lot of them, so read the article if you are interested)))
(((Conclusion: mice with mutations that make them age fast can be successfully helped with lots of substances. I wouldn't expect much of it to transfer to humans)))
Abstract follows:
The Senescence-Accelerated Mouse (SAM) strain was established in the Department of Senescence Biology, Chest Disease Research Institute, Kyoto University, as a novel murine model of senescence acceleration and age-associated disorders. This strain is actually a group of related inbred strains (recombinant inbred strain-like) including nine strains of accelerated senescence-prone, short-lived mice (SAMP) and three strains of accelerated senescence-resistant, long-lived mice (SAMR). Each SAMP strain shows relatively strain-specific age-associated pathologies. These characteristic pathological phenotypes are similar to those often observed in elder humans. They include senile osteoporosis, osteoarthritis, age-related deficits in learning and memory with/without forebrain atrophy, presbycusis, senile amyloidosis, age-related impairment of the immune response, and so on. The common aging characteristic of SAMP strains is senescence acceleration after normal development and maturation. We have made attempts to intervene the senescence acceleration and specifically in these pathologies: senile osteoporosis and the age-related deficits in learning and memory. These attempts, including caloric restriction, administration of nutrients, chemicals and traditional herbal medicines, show beneficial effects on the aging process of these mice. Similar interventions may prevent or control the onset and progress of age-associated disorders in other species and may have clinical relevance for humans.
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