Molecular Mechanisms of Aging and Research

<p>It increases lifespan. (C)</p> Signup and view all the answers

<p>To share blood supply between two conjoined animals. (B)</p> Signup and view all the answers

<p>Approximately 50 cell types are susceptible to accelerated aging effects. (C)</p> Signup and view all the answers

<p>It experiences rejuvenation effects. (A)</p> Signup and view all the answers

<p>Molecular mechanisms including free radicals and cellular lifespan. (C)</p> Signup and view all the answers

<p>It reduces epigenetic age. (D)</p> Signup and view all the answers

<p>Genetic inheritance (D)</p> Signup and view all the answers

<p>Accumulation of nuclear DNA damage. (C)</p> Signup and view all the answers

<p>Aging reflects a continued embryonic program. (C)</p> Signup and view all the answers

<p>Cellular senescence. (B)</p> Signup and view all the answers

<p>Decreased cognitive function. (D)</p> Signup and view all the answers

<p>Parabiosis. (D)</p> Signup and view all the answers

<p>Reduction in cellular lifespan. (C)</p> Signup and view all the answers

<p>Both intrinsic and extrinsic insults (D)</p> Signup and view all the answers

<p>Natural cessation of cell division after many cycles (C)</p> Signup and view all the answers

<p>It regulates proper healing by limiting fibrotic tissue development (D)</p> Signup and view all the answers

<p>It can be beneficial during tissue remodeling and development (D)</p> Signup and view all the answers

<p>It is the greatest risk factor for various diseases (D)</p> Signup and view all the answers

<p>Blocks the cell cycle (C)</p> Signup and view all the answers

<p>It lacks effective gene repair mechanisms (A)</p> Signup and view all the answers

<p>Increased somatic mutations are associated with aging (C)</p> Signup and view all the answers

<p>Chronic immune response triggers (B)</p> Signup and view all the answers

<p>Regulate functions in other tissues (B)</p> Signup and view all the answers

<p>It signals inflammation and neurological disorders (C)</p> Signup and view all the answers

<p>Alters metabolites and energy production (A)</p> Signup and view all the answers

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

<p>They can travel outside of cells affecting other tissues (B)</p> Signup and view all the answers

<p>Telomerase activity (B)</p> Signup and view all the answers

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

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

<p>They activate and proliferate more (B)</p> Signup and view all the answers

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

<p>SHLP2 (A)</p> Signup and view all the answers

<p>Stable cell cycle arrest (B)</p> Signup and view all the answers

<p>It is used in monotherapy for individuals unable to achieve glycemic control with diet and exercise. (B)</p> Signup and view all the answers

<p>Excreted unchanged through the kidneys. (C)</p> Signup and view all the answers

<p>To investigate its ability to slow aging and reduce senescent cell burden. (B)</p> Signup and view all the answers

<p>Its potential as a senolytic drug targeting senescent cells. (D)</p> Signup and view all the answers

<p>Approximately 2 hours. (A)</p> Signup and view all the answers

<p>Inhibiting the mTOR pathway (D)</p> Signup and view all the answers

<p>Senescence-Associated Secretory Phenotype, it promotes inflammation (B)</p> Signup and view all the answers

<p>Enhancing glycolysis and improving glucose uptake by muscles (A)</p> Signup and view all the answers

<p>By activating the PI3K-Akt signaling pathway (B)</p> Signup and view all the answers

<p>Down-regulating senescence markers and SASP factors (C)</p> Signup and view all the answers

<p>Decreased protein synthesis and enhanced autophagy (D)</p> Signup and view all the answers

<p>By inhibiting complex I of the electron transport chain (C)</p> Signup and view all the answers

<p>Reduces triglycerides and LDL cholesterol levels (A)</p> Signup and view all the answers

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

<p>Activates SIRT1, reducing cellular stress (B)</p> Signup and view all the answers

<p>It phosphorylates and inhibits transcription factors related to glucose production (A)</p> Signup and view all the answers

<p>Caenorhabditis elegans and mice (C)</p> Signup and view all the answers

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

<p>It has anticoagulant and fibrinolytic properties (B)</p> Signup and view all the answers

<p>By reducing protein synthesis (B)</p> Signup and view all the answers

<p>Increased AMP levels and activation of AMPK (A)</p> Signup and view all the answers

Suggests aging is caused by free radicals harming cells and tissues.

Harmful molecules resulting from cell processes that contribute to aging and diseases.

Human cells have a limited lifespan in cell culture.

Reducing calorie intake can increase lifespan (in animals like mice).

Joining two animals of different ages to share blood circulation to study aging.

Sharing blood influences aging in both mice (the younger gains health; older gets younger).

Many cells are susceptible to changes in aging when exposed to blood circulation.

Free radicals are partly produced from reactions involving oxygen and metals like iron in tissues (tissues).

Changes in gene expression without altering the DNA sequence, observed in aging mice.

Surgical procedure where the circulatory systems of two organisms are connected, used to study aging.

Aging is not a pre-determined, regulated process, but a result of accumulated harmful events.

Successful aging involves biomedical (physical, cognitive health) and psychosocial factors (psychological well-being).

Loneliness, a perceived sense of isolation, affects aging negatively, particularly in elderly and disabled populations.

A spectrum of alterations in DNA, including nuclear DNA damage, mitochondrial DNA changes, and abnormal DNA structures.

A severe type of DNA damage, specifically the breakage of both strands of a DNA double helix.

A state in cells where they stop dividing and can affect tissues and organs negatively during aging.

A cellular process triggered by DNA damage to prevent the transmission of damaged genetic information to offspring cells.

Control points in the cell cycle that halt cell division if DNA damage is detected.

DNA found in mitochondria, the cell's energy powerhouses. It's different from nuclear DNA and more susceptible to mutations.

Increased levels of reactive oxygen species that damage cellular components, including mtDNA.

Mitochondrial DNA released from damaged mitochondria into the surrounding fluids.

As we age, mtDNA becomes unstable leading to cellular damage triggering inflammation and impaired cell-to-cell communication.

Mitochondrial signaling molecules that regulate various functions.

Peptides produced within mitochondria from short open reading frames (sORFs) on mtDNA and can affect gene expression and intercellular communication.

Senescence is considered a cellular response to various stressors, such as DNA damage, oxidative stress, or oncogenic activation.

Replicative senescence is natural aging after many cell divisions, while premature senescence is triggered by stressors, leading to early aging.

Senescence plays a crucial role in development, tissue remodeling, and wound healing by eliminating unwanted cells and limiting fibrosis.

While beneficial in the early stages, prolonged senescence contributes to aging and disease by accumulating senescent cells that can release harmful substances.

Senescence can be targeted with drugs to potentially delay aging and reduce age-related diseases, suggesting a new avenue for anti-aging therapies.

A mitochondrial protein whose low levels are linked to worse cognition and aging in animals and humans. It also helps protect against Alzheimer's disease.

Another mitochondrial protein whose low levels are associated with poor metabolic health in humans. It plays a role in energy regulation.

A mitochondrial protein that acts as a chaperone, helping other proteins fold correctly. Low levels are associated with aging in mice and prostate cancer in humans.

Increased levels of cellular DNA in the cytoplasm of CD4+ T cells contribute to inflammation and aging, especially in older individuals.

These protective caps at the ends of chromosomes shorten with each cell division, marking the passage of time and influencing lifespan.

Changes in DNA methylation patterns with age, influencing gene expression and contributing to the aging process.

Cellular senescence is a process where cells stop dividing and enter a state of permanent arrest. It is triggered by stress or damage and contributes to aging by reducing the number of functional cells in tissues.

Metformin helps lower blood sugar by increasing insulin sensitivity, promoting glucose uptake in tissues, and boosting fatty acid oxidation.

Metformin gets cleared from the body quickly, with a half-life of about 2 hours. This means it's constantly being replaced.

The kidneys are the main route for eliminating metformin from the body. Only a small portion is broken down in the liver.

Metformin is a first-line treatment for type 2 diabetes, either alone or with other medications, to control blood sugar.

Metformin is under study for its ability to eliminate senescent cells, which may contribute to aging and age-related diseases.

Metformin reduces glucose production in the liver by inhibiting mitochondrial complex I of the electron transport chain.

Metformin increases AMP levels in the liver, activating AMPK, a key regulator of energy metabolism.

Metformin inhibits gluconeogenic gene expression through AMPK's action on transcription factors like CBP and CRTC2.

Metformin lowers blood sugar levels by reducing the liver's glucose production and improving insulin sensitivity.

Metformin has been shown to increase healthspan and lifespan in model organisms, suggesting broader benefits beyond diabetes.

Metformin can down-regulate senescence markers and SASP factors, reducing inflammation and damage caused by senescent cells.

Biguanides, like metformin, are effective insulin sensitizers commonly used in the treatment of type 2 diabetes.

Metformin improves peripheral glucose utilization, increasing glucose uptake by muscles and enhancing glycolysis.

Rapamycin, a drug initially used for organ transplant rejection, slows aging by inhibiting mTOR, a pathway involved in cell growth and metabolism. This reduces protein synthesis, promotes cell cleanup (autophagy), and reduces harmful effects of aging cells.

mTOR pathway controls cell growth and metabolism. Blocking mTOR with rapamycin slows aging by reducing protein synthesis, increasing recycling of cellular components (autophagy), and counteracting the detrimental effects of aging cells.

Resveratrol, found in red wine, protects against aging by activating telomerase, promoting cell function, and reducing cellular stress and inflammation. It works by activating SIRT1, a protein known to extend lifespan.

SIRT1, a protein activated by resveratrol, reduces cellular stress and inflammation, thus slowing down aging. It also helps cells stay young and functional.

Metformin, a drug for type 2 diabetes, also shows anti-aging properties. By reducing the activity of SA-β-gal, an indicator of aging cells, it can possibly help limit the buildup of aging cells that contribute to disease.

SA-β-gal is an enzyme found in high amounts in aging cells. Reducing its activity with drugs like metformin can potentially slow down the aging process.

Reducing calorie intake (caloric restriction) slows aging by activating sirtuins, proteins that promote cellular repair and stress resilience, reducing the negative effects of aging cells.

Sirtuins, activated by caloric restriction or compounds like resveratrol, promote cellular repair and stress resistance, thus promoting healthy aging.