Hot answers tagged senescence
13
The 'wear and tear' argument is most likely true but it is also interesting to reason about ageing as inevitable from the evolutionary point of view.
To set up the argument, we need two things:
First, each individual has got a 'reproductive potential' which is realised throughout life. This means a deleterious mutation which has an effect in early life, ...
11
From a certain point of view you could argue that our bodies have an inherently limited lifespan;
Telomeres are extensions to the end of chromosomes that prevent damage or loss of genetic information during cell division. Telomeres are not replaced (in normal cells), which gives rise to a replicative lifespan; the number of times a cell can divide before ...
10
Each individuals hair colour is determined by the particular pigment they produce (called melanin - the same stuff in your skin that makes you tan).
As the body ages this pigment (produced by the melanonocytes - cells that reside in the hair follicle) is produced less and less, until the hair is no longer coloured, and appears grey.
This is unique to each ...
10
It's worth noting that earlier this month a large body of resveratrol research was retracted:
The University of Connecticut, in what clearly seems like an attempt to get ahead of damaging news, has announced an “extensive”
investigation into research misconduct involving one of its
scientists, Dipak K. Das.
According to a press release, the ...
10
Caspase do not directly kill the cell, but rather activate a process known as apoptosis, or programmed cell death. The programmed part is there to distinguish it from other types of cell death, such as necrosis, which are more aspecific death processes.
Coming back to caspases, they are a series of proteasis, that can activate in cascade in response to a ...
9
Hydra are just one of the many organisms which are immortal. That is to say all their cells divide forever - there is no senescence (planned cell death) in any of their cells. Interestingly Hydrae that reproduce sexually age and die, but asexual reproduction appear to be immortal. Animals that are immortal more often reproduce asexually... this may only ...
8
Free radicals are damaging because their unpaired electrons (or not fully filled valence shell) makes them highly reactive species. They are often considered together with highly oxidizing "reactive oxygen species" (ROS) such as peroxides. They are especially problematic for cell membranes and DNA. In the latter they can react with (oxidize) heterocyclic ...
8
Gametes (sperm and ovum), which fuse to form a zygote, arise from germ cells [ spermatogonia and oogonia). Germ cells, like stem cells, are maintained carefully i.e the genome is preserved and transposition/recombination events are tightly controlled.
So these germ cells don't have shortened telomeres. Also, during early embryonic development the future ...
7
If you search clinicaltrials.gov (maintained by the NIH) for "resveratrol", you'll find 44 clinical trials, many of them ongoing or not yet started.
A recent review by Smoliga JM et al states in the abstract:
"Although the supporting research in laboratory models is quite substantial, only recently data has emerged to describe the effects of resveratrol ...
7
Well, Erickson et al (2011) attribute the increase in brain volume in the aerobic exercise group to brain-derived neurotrophic factor (BDNF).
Specifically (p. 3020):
In fact, we found here that changes in serum BDNF levels were
associated with changes in anterior hippocampal volume; an important
link because the hippocampus is rich in BDNF, and BDNF ...
6
I think it is the wrong question. You assume that eukaryotes developed from a single-cell organism with circular DNA. Then, clearly, there must have been an advantage of (newly) developing a linear genome. But eukaryotes could have developed from an organism with linear DNA, too. There are still a few bacterial species with linear chromosomes, so this is not ...
6
p16-INK4a is a part of a very important checkpoint mechanism. It's the "bad guy" in the context of aging because it induces senescence, and too much senescence leads to aging-related tissue degradation.
But senescence is important. It's one of the responses cells take when something goes wrong-- DNA damage, viral infection, telomere depletion, that sort of ...
6
There are many papers suggesting a link between AMPK (the major cellular sensor of the AMP/ATP ratio) and lifespan. As with most of these sorts of experiments, I think it is currently unclear precisely what the mechanism for this is, but AMPK regulates TORC1 and autophagy, both of which are also important for lifespan regulation. Here is a PubMed link to ...
6
Once could argue that we die because it is advantageous to get rid of mature individuals once they have reproduced. Because mature individuals have no more offspring to convey beneficial genes, those offspring which will benefit from knocking off their ancestors will have an evolutionary advantage.
6
Well, this needs to be broken down into two parts. Do Crocodilians age (undergo senescence), and are Crocodilians immortal (will only die of external causes)?
Are Crocodilians immortal?
- No. They appear to live about as long as humans before they die.
Measuring crocodile age is unreliable, although several techniques are used to derive a reasonable ...
4
There is a pretty good discussion on this topic in chapter 2 of Geriactric Medicine - An Evidence Based Approach (4th ed) by Cassel. This is the main reference for the info below which can hopefully add something to the answers already given.
In terms of views on ageing, there's evidence to support both:
general principles that may apply to it; and
it ...
4
Nice answer by Poshpaws +1. Free radicals can damage membranes (especially important for mitochondrial and endoplasmic reticulum membrane function), DNA (genes, telomeres, and mitochondrial DNA, eg), and microsomes. These are the things we consider with regard to ROS for our research on aging.
The role of diet is not clear. Smoking and alcohol may have ...
4
In a study on longevity in 121 countries, women tended to outlive men by about 5 years [1]. The suggested causes for this are numerous, some of which are temporally, geographically, or culturally specific.
On the terminology, sex tends to refer to the absolute biological differences, whereas gender relates more to differences in perception/lifestyle (for ...
4
Although many studies have shown that there are trade-offs between
longevity and reproduction, whether such trade-offs exist in humans
has been a matter of debate [1,2]. In many species, including humans,
males live shorter than females, which could be due to the action of
male sex hormones. Castration, which removes the source of male sex
...
4
This isn't so precisely focused on tortoises, but a general theory in evolutionary biology for why some animals live longer is K vs r selection theory.
The idea here is that animals will make a sort of evolutionary 'choice' and configure themselves to breed as numerously and quickly as they can. This is called 'r' selection, named after the constant that ...
3
Dementia with Lewy bodies (DLB): It is characterized anatomically by the presence of Lewy bodies, clumps of alpha-synuclein and
ubiquitin protein in neurons, detectable in post-mortem brain
histology.[1] Lewy Body dementia affects 1.3 million individuals in
the United States alone.
http://en.wikipedia.org/wiki/Dementia_with_Lewy_bodies
...
3
Looking at the articles referenced in the Wikipedia article, there's probably no direct physiological link between senescence and beta-galactosides. Lee et al (2006) and others before them have shown that the "hypothetical" protein is just regular lysosomal beta-galactosidase, which is present in higher concentrations in aging and stressed cells because the ...
3
Resveratrol has recently been shown to induce cellular senescence (at least at high concentrations, see here) which has the potential to accelerate ageing. Senescent cells display and highly inflammatory phenotype which could damage tissues if not removed. However, Resveratrol itself is rapidly metabolised and it may be these metabolites that have health ...
2
I can't rule it out, but it sounds a lot like trying to tune a piano with sledgehammer.
Neuronal LTP depends on protein translation, but so does absolutely everything else in the cell. Inhibiting protein synthesis at the ribosome will block the formation of all proteins, not just the ones responsible for LTP. Unless there's a link I don't know about ...
2
To clarify; administration of rapamycin (a drug) to lab organisms (including mice [1]) extends lifespan. Similarly, restricting the intake of nutrients to the minimum without causing malnutrition also extends lifespan in lab animals (including primates [2]).
Rapamycin inhibits the mTOR pathway (mammalian Target Of Rapamycin) - specifically mTORC1 (Complex ...
2
Rapamycin specifically inhibits the mTOR pathway (mTOR = mammalian target of rapamycin), which has numerous downstream functions including protein biogenesis, regulation of cell cycle, immune function and apoptosis. The upstream effectors of mTOR include growth factors and amino acid availability, so you can certainly see that the lifespan enhancing effects ...
2
This study found a statistically significant decline in NAD+:NADH ratios and in intracellular NAD+ with age in the organs of rats.
They discuss that the activation of PARP - the NAD-dependent enzyme Poly(ADP-ribose) polymerase-1 instrumental in DNA repair - increases in aging organs (heart, liver, kidneys). This depletes cellular NAD+ levels via ...
2
"WHY" we age is a different question from "HOW" we age. The "WHY" refers to ageing from an evolutionally standpoint, whereas the "HOW" refers to biology of ageing. As for the "WHY" I would read a few papers on the antagonistic pleiotropy hypothesis (click here). As for the "HOW", there is no definitive understanding of mechanisms of ageing. However, the ...
2
From my Immunology notes:
*Decrease in hematopoietic stem cells resulting in a reduction of Affector cells. Erythroid and myeloid progeny cells don't seem to be affected.
*Fewer pro-B cells, resulting in fewer affector B-cells.
*Lymphoid progenitors in the bone marrow and thymus mature.
*Lymphocytes in secondary lymphoid organs.
For the Innate system:
...
2
Progeria (and related) syndromes are essentially a collection of 'accelerated aging' phenotypes caused by single mutations; Progerin is a shortened version of the protein Lamin A, and is therefore not found in individuals without a loss-of-function mutation in the LMNA gene (the wiki page you reference). As far as we are aware these genes do not 'cause' ...
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