Steven Bussinger
Member
https://lpi.oregonstate.edu/sites/lpi.oregonstate.edu/files/pdf/newsletters/fw16.pdf#page=5
Reading between the lines here, Dr. Peat has cited the naked mole rat as an example of how CO2 increases longevity.
linus pauling institute naked mole rat at DuckDuckGo
Trying to post the text here:
Patterns in nature show that, in general, the
larger an animal is, the longer it tends to live.
With every doubling of species body mass, there
is roughly a 16% increase in maximum species
life span. T e giant tortoise, for instance, can live
well past 100 years old; a dormouse is lucky to
see past its fourth birthday.
“But there are outliers to this logarithmic
relation,” said institute Principal Investigator
Viviana Pérez, Ph.D. T e naked mole rat should,
by body mass, live to f ve years old, but it ends
up living a maximum lifespan of 31 years. Bats,
same thing: they should live to be around six,
but instead live a maximum of 34 years.
Pérez’s laboratory at the institute is focused
on studying these animal outliers, asking what
makes them so capable of that long life, of
defying the ecological norm. She’s honed in on
proteins, and their tendency to get “sticky” with
age. When proteins stick to each other, this is
known as protein aggregation. “You don’t want
your proteins to be aggregating,” says Pérez,
“you want each protein to be working
individually, doing its job.”
T is comparative biological approach has
important ties to human health and longevity.
Alzheimer’s and Huntington’s, for instance, are
both diseases where certain proteins go awry,
clump together, and cause problems. But in all
people, proteins are more prone to aggregation
as they age, even without one of these specif c
diseases. “T e quality of your proteins play an
important role in aging and disease,” said Pérez.
Her research asks the questions: how does
protein quality and resiliency impact longevity?
For long-living species like the naked mole rat,
what’s going on with protein aggregation? Do
they have cellular strategies for keeping their
proteins in good shape?
She recently received a federal grant from the
National Institutes of Health to further pursue
this line of inquiry. Previous research has shown
that the naked mole rat has potentially excellent
defenses against protein aggregation; now she’s
putting this theory to the test. Early results
from her cell culture experiments indicate that
cells from naked mole rats are more resilient to
the toxicity induced by protein aggregates than
cells of short-living species like mice. However,
and contrary to all expectations, naked mole rat
cells accumulate more of a specif c type of
protein aggregate (called polyglutamine; it’s the
protein implicated in Huntington’s disease) than
mouse cells. Moreover, cells from the naked
mole rat cause protein aggregates to accumulate
in a very specif c region of the cell: the perinuclear region, which is not observed in short-lived
mice. Based on these data, they hypothesize
that longevity is modulated not only through
resistance to protein toxicity, but also by the
capacity of the cell to clear protein aggregates
via a special “garbage deposit.”
T e next step is to f nd out which specif c
mechanisms within the naked mole rat are
responsible for this protective eff ect, and zero
in on them. Once mechanisms are identif ed,
then it opens up the possibility of modifying that
mechanism in another animal, like the mouse,
to see if one can impact the aging process and
disease trajectory. T is work, while still in the
early stages, could pave the way for a human
intervention that would maintain the quality of
proteins as people age, contributing to healthier
aging and possibly providing therapies for
protein-aggregation diseases, like Alzheimer’s.
“We know the naked mole rat is a weird animal,”
said Pérez, “we want to f nd out its secrets.”
Reading between the lines here, Dr. Peat has cited the naked mole rat as an example of how CO2 increases longevity.
linus pauling institute naked mole rat at DuckDuckGo
Trying to post the text here:
Patterns in nature show that, in general, the
larger an animal is, the longer it tends to live.
With every doubling of species body mass, there
is roughly a 16% increase in maximum species
life span. T e giant tortoise, for instance, can live
well past 100 years old; a dormouse is lucky to
see past its fourth birthday.
“But there are outliers to this logarithmic
relation,” said institute Principal Investigator
Viviana Pérez, Ph.D. T e naked mole rat should,
by body mass, live to f ve years old, but it ends
up living a maximum lifespan of 31 years. Bats,
same thing: they should live to be around six,
but instead live a maximum of 34 years.
Pérez’s laboratory at the institute is focused
on studying these animal outliers, asking what
makes them so capable of that long life, of
defying the ecological norm. She’s honed in on
proteins, and their tendency to get “sticky” with
age. When proteins stick to each other, this is
known as protein aggregation. “You don’t want
your proteins to be aggregating,” says Pérez,
“you want each protein to be working
individually, doing its job.”
T is comparative biological approach has
important ties to human health and longevity.
Alzheimer’s and Huntington’s, for instance, are
both diseases where certain proteins go awry,
clump together, and cause problems. But in all
people, proteins are more prone to aggregation
as they age, even without one of these specif c
diseases. “T e quality of your proteins play an
important role in aging and disease,” said Pérez.
Her research asks the questions: how does
protein quality and resiliency impact longevity?
For long-living species like the naked mole rat,
what’s going on with protein aggregation? Do
they have cellular strategies for keeping their
proteins in good shape?
She recently received a federal grant from the
National Institutes of Health to further pursue
this line of inquiry. Previous research has shown
that the naked mole rat has potentially excellent
defenses against protein aggregation; now she’s
putting this theory to the test. Early results
from her cell culture experiments indicate that
cells from naked mole rats are more resilient to
the toxicity induced by protein aggregates than
cells of short-living species like mice. However,
and contrary to all expectations, naked mole rat
cells accumulate more of a specif c type of
protein aggregate (called polyglutamine; it’s the
protein implicated in Huntington’s disease) than
mouse cells. Moreover, cells from the naked
mole rat cause protein aggregates to accumulate
in a very specif c region of the cell: the perinuclear region, which is not observed in short-lived
mice. Based on these data, they hypothesize
that longevity is modulated not only through
resistance to protein toxicity, but also by the
capacity of the cell to clear protein aggregates
via a special “garbage deposit.”
T e next step is to f nd out which specif c
mechanisms within the naked mole rat are
responsible for this protective eff ect, and zero
in on them. Once mechanisms are identif ed,
then it opens up the possibility of modifying that
mechanism in another animal, like the mouse,
to see if one can impact the aging process and
disease trajectory. T is work, while still in the
early stages, could pave the way for a human
intervention that would maintain the quality of
proteins as people age, contributing to healthier
aging and possibly providing therapies for
protein-aggregation diseases, like Alzheimer’s.
“We know the naked mole rat is a weird animal,”
said Pérez, “we want to f nd out its secrets.”
