Cell injury: cellular ageing: practice question

A Pathology question in the style of the NEET PG paper. Answer it first, then read why the right option is right and why each of the others is wrong.

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Pathology · Cell injury: cellular ageing

Sample item

A researcher compares fibroblasts from a young donor and an elderly donor in culture. The older cells stop dividing after fewer passages. Which mechanism most directly explains this replicative senescence?

Original practice item, not a recalled exam question. Nothing here is recorded.

The answer and the reasoning

A. Progressive telomere shortening that activates p53 and p21

Somatic cells lack telomerase, so telomeres shorten with each division; critically short ends are seen as DNA damage and activate p53 and p21, causing cell cycle arrest. Ageing is also driven by accumulated DNA damage and reduced sirtuin-mediated repair. Caloric restriction raises sirtuin activity and extends lifespan in experiments.

Option by option

  • A. Progressive telomere shortening that activates p53 and p21 (correct)

    Telomere attrition triggers a DNA damage response and permanent growth arrest.

  • B. Increased telomerase activity in somatic cells

    Somatic cells have little telomerase; high telomerase is a feature of germ cells, stem cells and cancer.

  • C. Reduced production of reactive oxygen species

    Ageing accumulates oxidative damage from reactive oxygen species rather than reducing it.

  • D. Upregulated sirtuin activity with enhanced DNA repair

    Ageing is associated with reduced, not increased, sirtuin activity.

Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.

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Questions about this Pathology question

What is the answer to this Pathology question?

The best answer is A, Progressive telomere shortening that activates p53 and p21. Somatic cells lack telomerase, so telomeres shorten with each division; critically short ends are seen as DNA damage and activate p53 and p21, causing cell cycle arrest.

Why is "Increased telomerase activity in somatic cells" not the answer?

Somatic cells have little telomerase; high telomerase is a feature of germ cells, stem cells and cancer.

Why is "Reduced production of reactive oxygen species" not the answer?

Ageing accumulates oxidative damage from reactive oxygen species rather than reducing it.

Why is "Upregulated sirtuin activity with enhanced DNA repair" not the answer?

Ageing is associated with reduced, not increased, sirtuin activity.

What concept does this question test?

It tests Cell injury: cellular ageing in Pathology. Ageing is also driven by accumulated DNA damage and reduced sirtuin-mediated repair. Caloric restriction raises sirtuin activity and extends lifespan in experiments.

How hard is this question?

We tag it as an application question: it asks you to use a fact on a patient or a finding. The tag is our own editorial judgement, not an official difficulty rating, so read the reason for every option, not only the answer.

How should I study Cell injury: cellular ageing?

Learn each disease as a bundle: cause, key histology, markers, and the clinical hallmark. Then use the flashcards and the other Pathology questions on this site to test what stuck.

Is this a real NEET PG question?

No. It is an original practice item (editorial status: sample, version 1). NextPrep does not publish recalled or leaked questions, and independent faculty review of this item has not been completed yet, so confirm important facts in a standard textbook.