My research all points to an increase in inflammation, mainly due to AGE etc build up and an aging gut with ever more of the wrong bacteria in it.

…Post-translational modifications are known to influence protein structure and function. Some of these modifications might affect proteins in detrimental ways and lead to their misfolding and accumulation. Reducing sugars play important roles in modifying proteins, forming advanced glycation end-products (AGEs) in a non-enzymatic process named glycation. Several proteins linked to neurodegenerative diseases, such as amyloid beta, tau, prions and transthyretin, were found to be glycated in patients…
http://www.ncbi.nlm.nih.gov/pubmed/20186922

…Protein glycation due to hyperglycemia resulting in misfolding and aggregation, which is known as one of the most important reasons of diabetes complications…MB-92 showed the greatest potential for inhibition of glycation and oxidation products…and to control protein glycation, misfolding and aggregation…
http://www.ncbi.nlm.nih.gov/pubmed/26733359

Glycation is the reaction of a reducing sugar with proteins and lipids, resulting in myriads of glycation products, protein modifications, cross-linking, and oxidative stress. Glycation reactions are also elevated during metabolic dysfunction such as in Alzheimer’s disease (AD) and Down’s syndrome. These reactions increase the misfolding of the proteins such as tau and amyloid-β (Aβ), and colocalize with amyloid plaques…AGE colocalized with amyloid plaques. In summary, we demonstrate the glycation of Aβ and plaques by metabolic compounds. Thus, glycation potentially links metabolic dysfunction and Aβ misfolding…
http://www.ncbi.nlm.nih.gov/pubmed/22406446

Metals like iron etc catalyse and thus greatly speed up the the formation of AGEs.
Due to the slow turnover of the ECM the rate of formation of AGE soon outstrips the rate at which they are removed from the body.
The lack of stem cell activity is related, in that the the buildup of extra/intracellular junk blocks the signal to turn into new brain, liver etc cells.

Some examples of what happens when we go of the source and these metal are removed:

Novel molecular targets of the neuroprotective/neurorescue multimodal iron chelating drug M30 in the mouse brain.

The novel multifunctional brain permeable iron, chelator M30…was shown to possess neuroprotective activities in vitro and in vivo, against several insults applicable to various neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis…

chronic administration of M30 resulted in up-regulation of hypoxia-inducible factor (HIF)-1α protein levels in various brain regions (e.g. cortex, striatum, and hippocampus) and spinal cord of adult mice.…

M30 differentially induced HIF-1α-dependent target genes, including vascular endothelial growth factor (VEGF), erythropoietin (EPO), enolase-1, transferrin receptor (TfR), heme oxygenase-1 (HO-1), inducible nitric oxide synthase (iNOS), and glucose transporter (GLUT)-1. In addition, mRNA expression levels of the growth factors, brain-derived neurotrophic factor (BDNF) and glial cell-derived neurotrophic factor (GDNF) and three antioxidant enzymes (catalase, superoxide dismutase (SOD)-1, and glutathione peroxidase (GPx)) were up-regulated by M30 treatment in a brain-region-dependent manner…

…M30 induced a differential enhanced phosphorylation of protein kinase C (PKC), mitogen-activated protein kinase (MAPK)/ERK kinase (MEK), protein kinase B (PKB/Akt), and glycogen synthase kinase-3β (GSK-3β). Together, these results suggest that the multifunctional iron chelator M30 can up-regulate a number of neuroprotective-adaptive mechanisms and pro-survival signaling pathways in the brain that might function as important therapeutic targets for the drug in the context of neurodegenerative disease therapy.
http://www.ncbi.nlm.nih.gov/pubmed/21570450…
LR-90 a new advanced glycation endproduct inhibitor prevents progression of diabetic nephropathy…and was a more potent metal chelator than pyridoxamine and aminoguanidine…
http://www.ncbi.nlm.nih.gov/pubmed/21570450

…LR-90 reduces in vivo AGE accumulation, AGE-protein cross-linking and protein oxidation…
The AGE inhibitory and therapeutic effects of LR-90 could be attributed, at least in part, to its ability to react with reactive carbonyl species and/or potent metal chelating activity that inhibits glycoxidative-AGE formation…
http://www.longecity.org/forum/topic/57939-do-age-blockers-a…8;p=765347

Ninety Percent Reduction in Cancer Mortality after Chelation Therapy With EDTA
http://www.longecity.org/forum/topic/60850-ninety-percent-re…with-edta/

Tiron is able to chelate iron inside the mitochondria, giving 100% protection against UV.
In this study UV caused the free iron, but iron buildup is a known problem.
http://www.longecity.org/forum/topic/68047-investigating-tir…tioxidant/

Chelation therapy/glycation research seems to be actively discouraged…?!!!

Lastly; Low dose Nilotinib looks to be the best therapy currently available for:
Clearing misfolded proteins.
Preventing amyloid secretion into the extracellular space between neurons.
Facilitating the mitophagy of old, sickly mitochondria.
http://www.longecity.org/forum/topic/84008-nilotinib-group-buy/page-11

Logic

You could say that a cars fail to function owing to an intrinsic property of its human maintenance system — but the failure is more immediately a result of accumulated damage.