Aging is the common background of several aging-related disorders, such as AD and PD. To answer the question raised here, one has to first ask what causes aging: genetics (RAS), immune senescence, free radical accumulation, DNA damage, etc. Enhancing patients' well-being is necessary for the therapeutic approach of AD and PD.

View all comments by Yue Huang

Aging increases the probability of virtually all common diseases within the demographic the individual(s) live in. The system has years of wear and tear with antibodies being selected for adaptive immunity. Years of eating, breathing (pollutants, microorganisms etc...) and moving.

Aging is a multifactorial phenomenon set on a continuum, and as such genetics and environment alone are not even enough to find strong causal triggers of age-related dementia. Working out the genetic-environmental link is extremely difficult.

View all comments by Jacob Mack

Aging is divided into

1. Primary aging—due to inherent progressive decreased activities of the genes that regulate the cells.

2. Secondary aging (accelerated aging)—primarily due to oxidative stress. Oxidative stress is mainly caused by external factors such as environmental factors, toxic materials, ionizing radiations, or any disease or condition that alters the vascular endothelium and the cell wall membrane. These altered conditions allow the entry of substances that displace the zinc from cell-specific carbonic anhydrase enzymes, leading to their decreased levels, hence, leading to cellular death.

What the medical field does not know is about carbonic anhydrase enzymes, their molecular reactions, and functions at the cellular level.

Carbonic anhydrase enzymes are ancient zinc enzymes which are further divided into α, which belongs to mammals and is thought to be 200 to 300 million years old; the β, which belongs to plants and is thought to be 3.5...  Read more

Aging is divided into

1. Primary aging—due to inherent progressive decreased activities of the genes that regulate the cells.

2. Secondary aging (accelerated aging)—primarily due to oxidative stress. Oxidative stress is mainly caused by external factors such as environmental factors, toxic materials, ionizing radiations, or any disease or condition that alters the vascular endothelium and the cell wall membrane. These altered conditions allow the entry of substances that displace the zinc from cell-specific carbonic anhydrase enzymes, leading to their decreased levels, hence, leading to cellular death.

What the medical field does not know is about carbonic anhydrase enzymes, their molecular reactions, and functions at the cellular level.

Carbonic anhydrase enzymes are ancient zinc enzymes which are further divided into α, which belongs to mammals and is thought to be 200 to 300 million years old; the β, which belongs to plants and is thought to be 3.5 billion years old; and γ, which belongs to the methane-producing bacteria and is thought to be about four billion years old. These carbonic anhydrase enzymes are structurally distinct from each other except they contain the same zinc ion and catalyze the same reaction: H2O + CO2 (reversible) H + HCO3.

In α carbonic anhydrase enzymes, aside from uses and other functions that are known by the medical community, they produce hydrogen ions acted upon by the cytochrome system found in the mitochondria and utilized as

1. Fuel of the ion pump that maintains the integrity of the cell wall membrane.

2. H + (hydrogen ion) + ADP (adenosine diphosphate)—ATP (adenosine triphosphate) fuel for all other cellular functions.

3. Glucose + O2 (oxygen)—H2O + CO2 = (O2)-2 (reactive oxygen 1 to 5 percent is produced).

Hydrogen ion is needed to neutralize the oxygen free radicals produced during aerobic respiration. Decreased levels of carbonic anhydrase enzymes lead to decreased levels of hydrogen ions produced to neutralize all reactive radicals, hence, oxidative stress.

In aging, there is a progressive decrease in levels of cell-specific carbonic anhydrase enzymes.

References:
U.S. Patent application # 11/801870, which is a continuation in part of U.S. Patent # 7256184 "Treatment of Aging Disorders in Humans." See http://www.uspto.gov.

View all comments by Victorio Rodriguez