Correct option is D
The correct answer is option (d). The statement about female mice with a mutation in IGF-1 and IGF-2 showing reduced lifespan is incorrect. Mutations in IGF-1 and IGF-2 that reduce their activity are actually associated with increased lifespan, not reduced lifespan. This is because IGF-1 signaling has been linked to aging and diseases related to aging. Lowering IGF-1 activity tends to extend lifespan by delaying the aging process and reducing the risk of age-related diseases like cancer.
Now, let’s review why the other options correctly characterize aging:
Option (a): The insulin/IGF-1 signaling pathway is well-known to play a significant role in controlling lifespan. Reduced activity of IGF-1 signaling is generally associated with longer lifespan and delayed aging in model organisms, such as worms, flies, and mice.
Option (b): Oxidative stress is a key factor contributing to aging. Over time, the accumulation of free radicals causes cellular damage, which accelerates the aging process. However, increasing resistance to oxidative stress does not inherently increase lifespan but can help slow down the aging process and reduce the incidence of age-related diseases.
Option (c): Shortening of telomeres is one of the most prominent features of aging. Telomeres shorten with every cell division, and once they become critically short, cells either undergo senescence or apoptosis (cell death). This contributes significantly to aging and the development of age-related diseases.
Thus, option (d) is incorrect because a mutation in IGF-1 and IGF-2 that reduces their activity would actually increase lifespan, not decrease it.
Information Booster:
Insulin/IGF-1 signaling system: This pathway regulates growth and metabolism, and is critical in controlling lifespan. Reducing IGF-1 activity has been shown to increase lifespan in several species, including humans and mice, due to reduced cellular damage and delayed aging.
Oxidative stress and aging: Oxidative stress is a condition where the body's cells are damaged by free radicals, which are highly reactive molecules. These free radicals cause DNA damage and cellular dysfunction, leading to aging and the development of diseases such as Alzheimer's and cancer. Resistance to oxidative stress is one of the mechanisms that can help slow aging but does not necessarily increase lifespan in a linear way.
Telomere shortening: Telomeres protect chromosomes during cell division, but they shorten with each division. Over time, the shortening of telomeres contributes to cell aging and the eventual loss of the ability to divide, which plays a central role in aging.
IGF-1 and lifespan: Mutations that reduce the activity of IGF-1 or its receptor have been linked to increased longevity in model organisms. This pathway regulates growth, metabolism, and aging, and its reduction leads to decreased cancer risk and delayed aging.
