Aging and Insulin Signaling in C. elegans

<p>2 weeks (D)</p> Signup and view all the answers

<p>It is associated with stress resistance and longevity. (C)</p> Signup and view all the answers

<p>It is activated. (A)</p> Signup and view all the answers

<p>They can mimic aspects of dauer larvae longevity. (C)</p> Signup and view all the answers

<p>Activation of DAF-16/FOXO. (B)</p> Signup and view all the answers

<p>Simple genetic changes (A)</p> Signup and view all the answers

<p>It regulates insulin signaling pathways. (B)</p> Signup and view all the answers

<p>It extends lifespan by approximately 40%. (B)</p> Signup and view all the answers

<p>It integrates stress signals. (C)</p> Signup and view all the answers

<p>They protect DNA during cell replication. (D)</p> Signup and view all the answers

<p>It induces cellular senescence. (A)</p> Signup and view all the answers

<p>The maximum number of cell divisions before senescence. (B)</p> Signup and view all the answers

<p>Targeting insulin signaling pathways. (C)</p> Signup and view all the answers

<p>Accumulation of senescent cells. (A)</p> Signup and view all the answers

<p>They are implicated in oxidative stress mitigation. (B)</p> Signup and view all the answers

<p>Potential heart and tissue damage. (A)</p> Signup and view all the answers

<p>They are associated with longer-lived breeds. (D)</p> Signup and view all the answers

<p>It contributes to cellular dysfunction. (C)</p> Signup and view all the answers

<p>To mimic the effects of caloric restriction pharmacologically. (D)</p> Signup and view all the answers

<p>Eliminating senescent cells (A)</p> Signup and view all the answers

<p>By activating genes that produce antioxidants (B)</p> Signup and view all the answers

<p>They assist in the folding and refolding of proteins. (A)</p> Signup and view all the answers

<p>Formation of amyloid plaques (D)</p> Signup and view all the answers

<p>Accumulation of misfolded proteins (B)</p> Signup and view all the answers

<p>Induces a starvation-like state in well-fed conditions (A)</p> Signup and view all the answers

<p>Proteasomes (A)</p> Signup and view all the answers

<p>It contributes to the accumulation of aggregated proteins. (B)</p> Signup and view all the answers

<p>Addressing oxidative stress and DNA integrity (B)</p> Signup and view all the answers

<p>AD shows accelerated brain shrinkage. (C)</p> Signup and view all the answers

<p>Formation of protein aggregates (B)</p> Signup and view all the answers

<p>Promoting chronic inflammation (B)</p> Signup and view all the answers

<p>Enhancing selective telomerase activity in stem cells may help maintain regenerative potential. (C)</p> Signup and view all the answers

<p>1,000 (A)</p> Signup and view all the answers

<p>It forms plaques that disrupt brain function. (D)</p> Signup and view all the answers

<p>Beta-secretase (B)</p> Signup and view all the answers

<p>Through continuous self-repair. (A)</p> Signup and view all the answers

<p>Early-Onset Alzheimer's (D)</p> Signup and view all the answers

<p>Regular physical activity (A)</p> Signup and view all the answers

<p>Plaque accumulation leads to cognitive decline. (C)</p> Signup and view all the answers

<p>Alpha-secretase cleavage (D)</p> Signup and view all the answers

<p>It forms new neural pathways. (C)</p> Signup and view all the answers

<p>It forms neurofibrillary tangles. (B)</p> Signup and view all the answers

<p>Icelandic allele (C)</p> Signup and view all the answers

<p>Targeting the clearance of Aβ plaques. (C)</p> Signup and view all the answers

<p>They are post-mitotic and cannot regenerate. (B)</p> Signup and view all the answers

<p>Brain shrinkage due to neuronal loss. (B)</p> Signup and view all the answers

Protective caps at chromosome ends get shorter with each cell division.

A pathway that controls metabolism and lifespan, similar in C.elegans and humans.

A transcription factor activated by reduced insulin signaling, promoting longevity.

A small worm model organism used to study aging due to its short life cycle.

A developmental stage in C. elegans where it becomes dormant, promoting stress resistance and longevity.

Maintaining the proper functioning of the DNA and preventing cell damage.

High insulin signaling reduces lifespan. Low insulin signaling extends lifespan.

A short life cycle (approx. 2 weeks) making it a powerful model organism to study aging.

Reduced insulin signaling leads to increased lifespan in organisms, like C. elegans, due to the activation of DAF-16.

A FOXO transcription factor that activates over 100 genes, producing antioxidants and protecting against oxidative stress.

Reduces insulin signaling, mimicking starvation's effect on lifespan, often extending lifespan in rodents.

A protein that responds to cellular stress, like damage, by initiating DNA repair, senescence, or apoptosis (programmed cell death).

Permanent cell-cycle arrest; protecting against tumors but contributing to age-related tissue damage.

Repeated DNA sequences at chromosome ends that protect DNA integrity but shorten with each cell division.

The maximum number of cell divisions a normal cell can undergo before entering senescence.

An enzyme that rebuilds telomeres, allowing unlimited cell divisions, typically found in stem cells and cancer cells.

Aging reduces the regenerative capabilities of stem cells, contributing to age-related decline.

Accumulation of harmful molecules, increasing cellular dysfunction in aging.

A mutation that reduces insulin signaling and extend lifespan in model organisms (like C. elegans) due to its relationship with DAF-16.

Senescence initially protects against cancer but with age and accumulation can lead to aging-related decline (tissue dysfunction and inflammation).

A protein similar to insulin, whose levels correlate with longevity in various species, especially dogs.

Non-dividing cells that accumulate with age and negatively affect tissue function by contributing to stem cell depletion and secreting harmful factors.

Drugs targeting and eliminating senescent cells to reduce their harmful effects on tissues.

The dynamic process of maintaining the proper function, balance, and quality of the proteome by ensuring proteins are correctly synthesized, folded, transported, and degraded.

Proteins that assist in folding/refolding misfolded proteins, often induced under stress.

Degrade soluble, misfolded proteins tagged by ubiquitination.

Removes larger aggregates or dysfunctional organelles by encapsulating them in autophagosomes, which are then fused with lysosomes for degradation.

Extracellular deposits primarily composed of amyloid-beta (Aβ) peptides, implicated in Alzheimer's Disease.

Intracellular aggregates of hyperphosphorylated tau protein, disrupting microtubule function in Alzheimer's Disease.

Transcription factors activated by reduced insulin signaling, promoting longevity by triggering the expression of genes that enhance survival.

Aggregates of alpha-synuclein protein that form Lewy bodies, contributing to neurodegeneration in Parkinson's Disease.

Aggregates of alpha-synuclein protein found outside neurons, contributing to neurodegeneration in Parkinson's Disease.

The human brain operates on about 10–15 watts of energy, comparable to a dim lightbulb, demonstrating its remarkable efficiency.

The human brain's computational efficiency surpasses supercomputers, highlighting its remarkable ability to process information with minimal energy.

As we age, the efficacy of chaperones, proteasomes, and autophagy declines, leading to an accumulation of damaged or aggregated proteins.

The connections between neurons where information is transmitted. Each neuron forms an average of 1,000 synapses.

The ability of the brain to change and adapt its structure and function in response to learning and experience.

Neurons are post-mitotic, meaning they don't divide or regenerate after early adulthood. Unlike other cells, they have a lifespan as long as the individual.

Neurons constantly repair themselves to stay functional. Damage or malfunction can lead to neurodegenerative diseases.

Active engagement in learning strengthens and rewires synaptic connections, while passive learning is less effective.

A transmembrane protein involved in neuronal development and synaptic plasticity. Its abnormal processing leads to the formation of amyloid-beta (Aβ) plaques, associated with Alzheimer's.

The buildup of amyloid-beta (Aβ) plaques in the brain triggers a cascade of events, worsening Alzheimer's disease.

Enzymes that cleave APP, a protein involved in Alzheimer's. Beta-secretase produces harmful Aβ peptides, while alpha-secretase is considered safe.

The 42-amino-acid form of amyloid-beta peptide, known to be particularly harmful in Alzheimer's disease.

Specific mutations in the APP gene can increase the production of harmful Aβ42, leading to early-onset Alzheimer's.

Tau is a protein that forms tangles inside neurons, potentially contributing to Alzheimer's. While tau mutations are linked to other dementias, they don't directly cause familial Alzheimer's.

The role of Aβ in late-onset Alzheimer's is less clear than in early-onset AD.

Current research focuses on clearing Aβ plaques, stabilizing tau, and preventing the production of harmful Aβ peptides. However, finding safe and effective treatments is a challenge.