BDNF; Aging and Anti-Aging

Noradrenalin up regulates the Muller cell ( a retinal glial or helper cell of retinal nerves and nerve endings) production of BDNF (brain derived neurotrophic factor). Retinal degeneration occurs in elderly persons, the same age group cohort that develops other neurodegenerative diseases that BDNF prevents.

Noradrenalin is produced in high levels by HIIE (high intensity interval exercise.)

An early defect, preceding Alzheimer's disease by 20 years, is intracranial sympathetic (noradrenalin) tone loss that is associated with reduced heart rate variability, low BDNF levels and lower aerobic exercise capacity.  

Increased BDNF level, especially associated with noradrenalin increase, should protect the retina and brain.  HIIE of 4 minutes increases noradrenalin by 17 fold and last 19 minutes post exercise.  The use of green tea extract, an o methyl transferase inhibitor (enzyme that degrades stimulants) prolongs the basal (resting) rate of noradrenalin and may also be helpful.  Lastly, endothelial (blood vessel lining cells) cells produce BDNF, and taste bud receptor cells produce BDNF and is responsible for the continuous synapticity or connection hookup of the nerve to the taste bud.  Noradrenalin may up regulate the mRNA (DNA template that makes gene product proteins) of BDNF directly.  Green tea extract will be an indirect agonist (increases action) by increasing noradrenalin duration of activity by blocking its enzymatic break down.  HIIE would pulse or strengthen the effect of both.

Age related conditions are negatively impacted by BDNF neurodegenerative change.  

First in sympathetic and autonomic systems.  

Second in their end organs, 

retina, macular neuro-degeneration, 

taste, lack of connection or hook up of nerves to taste buds, 

appetite, a function of bone marrow produced BDNF, 

brain, mood and cognitive disconnection syndrome, and

heart, where low BDNF levels reduces the relaxation and contraction limits of the heart muscle cell and reduces the pump function of the heart reducing activity levels.

Conjecture.

Aging is degeneration of the network within and between cells.

Lack of BDNF allows degeneration.

Normal or increased BDNF reverses, stabilizes or slows degeneration.

A negative BDNF lifestyle and inflammation within cells and between cells degrades the individual's memory, mood and metabolism.

A positive BDNF lifestyle and anti-inflammatory strategy could reverse, stabilize or slow the disconnection syndrome that degrades the individual's memory, mood and metabolism. (Vision, hearing, taste, appetite, cardiac output)

Conjecture 2.

The elderly during and post autonomic, sympathetic intracranial nerve function decline might be rescued with supplementation of lifestyle agonist known to increase BDNF.

Noradrenalin; green tea extract, stimulant therapy.

Lactate; LR iv, Mag Lactate. (Lactate producing exercise increase BDNF production )

Intermittent weekly fasting; MCT oil. Axona to provide beta hydroxybutyrate.

HIIE; blood restricted exercise to produce lactic acid with low intensity exercise.

The core of this can be accomplished with my 3,2,1 plan at LivermanHealthAdvice.blogspot.com.

Müller Cells as a Source of Brain-derived Neurotrophic Factor in the Retina: Noradrenaline Upregulates Brain-derived Neurotrophic Factor Levels in Cultured Rat Müller Cells - Springer

http://link.springer.com/article/10.1007%2Fs11064-005-7936-7

Abstract

Müller cells, the predominant glial cells in the retina, are thought to play important roles in the survival of retinal neurons. Previous studies have demonstrated that Müller cells express brain-derived neurotrophic factor (BDNF), which has a pronounced neurotrophic effect on retinal ganglion cells. In this study, we investigated whether Müller cells express and release BDNF in culture. Reverse transcriptase-PCR, immunocytochemistry and Western blotting revealed that Müller cells produce BDNF mRNA and protein. Using the enzyme-linked immunosorbant assay, BDNF protein levels in Müller cells and their conditioned medium were quantified, demonstrating that Müller cells produce and release high levels of BDNF. Noradrenaline administration caused an upregulation of BDNF mRNA and protein expression by cultured Müller cells. These results suggest that Müller cells may act as an endogenous source of BDNF in the retina. Furthermore, induction of BDNF expression by adrenergic agonists may provide a therapeutic approach to retinal neurodegenerative disorders.