Nicotinamide adenine dinucleotide, a coenzyme critical for cellular energy metabolism that declines with age. NAD+ precursors like NMN and NR are studied as longevity interventions.

Mechanistic target of rapamycin, a key nutrient-sensing pathway that regulates cell growth and aging. Inhibiting mTOR (e.g., with rapamycin) has shown lifespan extension in multiple organisms.

A class of drugs that selectively eliminate senescent (aged, dysfunctional) cells to reduce inflammation and improve tissue function.

What is Epigenetic clock?

A biomarker based on DNA methylation patterns that estimates biological age, often more predictive of health outcomes than chronological age.

The period of life spent in good health, free from chronic diseases and disability associated with aging.

An immunosuppressant drug that inhibits the mTOR pathway. Research shows rapamycin may extend lifespan and improve age-related health outcomes in multiple species.

What is Biological age?

A measure of how well or poorly your body is functioning relative to your chronological age, assessed through biomarkers such as DNA methylation, telomere length, and blood panels.

What is Caloric restriction?

A dietary regimen that reduces calorie intake without malnutrition. Caloric restriction is one of the most studied interventions shown to extend lifespan across species.

Protective caps at the ends of chromosomes that shorten with each cell division. Telomere length is associated with aging and age-related diseases.

A state in which cells permanently stop dividing but resist death, accumulating with age and secreting inflammatory factors that damage surrounding tissue.

A second-generation epigenetic clock that predicts time to death and is considered one of the most accurate measures of biological aging.

What is Inflammaging?

Chronic, low-grade inflammation that increases with age and contributes to the development of age-related diseases including cardiovascular disease, diabetes, and neurodegeneration.

The large-scale study of proteins in biological systems. In longevity research, proteomics identifies blood protein signatures that predict biological age and disease risk.

What is Yamanaka factors?

A set of four transcription factors (Oct4, Sox2, Klf4, c-Myc) that can reprogram adult cells to a pluripotent state. Partial reprogramming with Yamanaka factors is being explored to reverse cellular aging.

Nicotinamide mononucleotide, a precursor to NAD+ that is widely studied as a supplement to boost cellular energy and combat age-related decline.

A gene-editing technology that allows precise modifications to DNA. In longevity research, CRISPR is used to study and potentially modify genes associated with aging.

A cellular housekeeping process where cells break down and recycle damaged components. Declines with age and is stimulated by fasting.

What is Intermittent fasting?

An eating pattern that cycles between periods of fasting and eating. Various protocols (16:8, 5:2) are studied for metabolic, cardiovascular, and longevity benefits.

What is Zone 2 cardio?

Low-intensity aerobic exercise performed at roughly 60–70% of maximum heart rate, primarily using the aerobic energy system. Associated with mitochondrial health and longevity.

Geographic regions identified by researchers where people consistently live longer and healthier lives than average, including Sardinia, Okinawa, and Loma Linda.

Do obesity and Alzheimer's disease share a connection?

Researchers have found important connections between obesity and Alzheimer’s disease (AD), suggesting that the biochemistry of these two conditions overlaps significantly. While obesity is known to contribute to various metabolic disorders, the relationship between obesity and Alzheimer’s is complex. Despite intriguing biological links, large studies show that obesity does not directly increase the risk of developing Alzheimer’s as clearly as it does for type 2 diabetes. This raises questions about why many people with obesity do not go on to develop Alzheimer’s, even though research has identified several potential mechanisms that could connect the two.

Understanding the relationship between obesity and Alzheimer’s matters for anyone interested in healthy aging. With the number of older adults increasing, the prevalence of Alzheimer’s is expected to rise, affecting memory and cognitive function. Currently, about 11% of Americans over 65 are diagnosed with Alzheimer’s, while obesity rates among older adults have nearly doubled in recent decades. The shared metabolic disturbances between obesity and Alzheimer’s, such as mitochondrial dysfunction and oxidative stress, may contribute to cognitive decline. Addressing metabolic health could be crucial for reducing the risk of neurodegenerative diseases.

The research reviewed highlights early-stage findings that suggest a link between obesity and Alzheimer’s through shared metabolic mechanisms. However, the evidence is still developing, and while there are compelling biochemical connections, we need more robust epidemiological data to fully understand this relationship. As of now, the evidence does not support a direct causal link between obesity and Alzheimer’s in the same way it does for type 2 diabetes.

For those looking to maintain cognitive health, focusing on metabolic health through a balanced diet and regular physical activity may be beneficial. While weight loss can improve metabolic conditions, it’s essential to approach weight management holistically, considering overall health and lifestyle rather than just weight alone.

Source: fightaging.org