Hello Vikas,

There are several major areas of aging research. Genetics and the interaction of genes with environment - epigenetics and the social aspects of aging and how they affect biological aging. I think you need to focus on one of these area, first, then the latest discoveries will be more relevant. For example, if you wish to study the aging brain and nutrients, the here is a link that could be of interest: Article A nutrigenomics approach for the study of anti-aging interve...

Not easy to answer your question in one sentence

Each dimension of aging research has its own importance

Amended on 16 March 2018

I have previouly reported uniquely about the life span of humans by using human serum biotinidase activity, which has shown the negative correlation with the human age (please see file; J Chrom B rat BIN LIP Km). Human life span seems to be 750 years by using non-parametric statistics with linear regression line (my unpublished observation; please see also the file, Feed by Measure).

Further, I must add that Apoptosis (found in Nematode Caenorhabditis elegans), Autophagy (found in Yeast Saccharomyces cerevisiae), Telomere (found in Insect Drosophila melanogaster and in Corn or Maize Zea mays), Telomerase (found in Ciliophora Tetrahymena pyriformis) and Caspase (found in Nematode Caenorhabditis elegans and Insect Drosophila melanogaster) are not truely working or not present in the humans by analyzing cellular proteins using the new proteomics (please see file; HepG2 fucoidan). Interstingly, the Ubiquitin-Proteasome system (UPS; ATP-dependent protein metabolic system: found in Human Reticulocyte and in Archaeum Thermoplasma acidopilum) is actively working in humans, although the Ubiquitin-Proteasome system is not linked to cancer. UPS seems to be linked to some brain-related diseases, but not linked to ageing.

I am now considering that the infection frequency or amount of virus and bacteria onto the aged persons may be strongly linked to ageing phenomena. Therefore, fucoidan (sulphated poly-L-fucose) seems to be the drug for antiageing, since fucoidan can reduce infected virus and bacteria.

Fucoidan effect on HCC is mainly due to reduction of HCV and HIV-1 (please see again; HepG2 Fucoidan). In relation to this effect of fucoidan, it is interesting that the brown algae “Kombu” (sea tangle of Laminaria japonica) has been the Longevity foodstuff in Japan.

By the way, I have searched for the lysosomal enzymes in my protein database.

Fetal hepatocyte Hc has Prenylcysteine oxidase 1 at 4.1μg/mg of cell protein.

Hepatoma HepG2 has no such enzymes. But, healed normal HepG2 by fucoidan has Cathepsin F at 0.08 μg/mg of cell protein and Vacuolar ATP synthase subunit D homolog at 0.39 μg/mg of cell protein (Total lysosomal protein 0.47 μg/mg of cell protein).

Liver tissue (pseudo-liver cancer) has N-Acetylglucosamine-6-sulfatase/G6S at 1.9 μg/mg of tissue protein and Lysosomal alpha-glucosidase/Acid maltase at 4.1 μg/mg of tissue protein (Total lysosomal protein 6.0 μg/mg of tissue protein).

LC tissue (with leprosy) has N-Acetylglucosamine-6-sulfatase/G6S at 3.2, Glycosylceramidase/Acid beta-glucosidase at 0.28, and Cathepsin B at 3.2 μg/mg of tissue protein, respectively (Total lysosomal protein 6.7 μg/mg of tissue protein).

HCC tissue (with PBC) has no such proteins.

LC tissue (named No.6) has Proactivator polypeptide/Prosaposin/Cerebroside sulfate activator at 1.8, Lysosome Arylsufatase A/ASA at 0.64, and Arylsufatase B/ASB at 3.9 μg/mg of tissue protein, respectively (Total lysosomal protein 6.3 μg/mg of tissue protein). But, HCC tissue (named No.6) has no such proteins.

Lysosome seems to be important role in glycoprotein-glycolipid-glycosaminoglycan metabolism in normal cells. It is interesting that Cancer HCC tissues seem to lose Lysosome and/or Lysosomal membranes. Lysozome seems to be not linked to ageing.

Maybe the following papers will help you: