Alzheimer´s Disease
It is clinically characterized by a deterioration of memory and other cognitive domains that leads to death within 3 to 9 years after diagnosis, being the most common form of dementia [
5].
Although a battery of neuropsychological tests are often used in making a clinical diagnosis of Alzheimer´s Diseases (AD), diagnosis still relies in clinical assessment [
6]. This progressive neurodegenerative disorder estimated to affect 5.1 million individuals in 2007 in USA. Unfortunately there are no affordable biomarkers in the diagnosis of disease cases, or in following disease progression and response to treatment as well. Therefore the unavailability of reliable biomarkers is a serious shortcoming.
Given the multifactorial nature of the disease, it is unlikely that a single biomarker will meet the needs for clinical diagnosis; beside that it is a formidable task to reach the appropriate sensibility and sensitivity.
AD is considered a multifactorial disease because the postmortem pathological diagnosis of an AD brain relies on unspecific histological findings as the presence of senile plaques neurofibrillary tangles. These senile plaques are composed of β-amyloid (Aβ), a proteolytic fragment of the Amyloid precursor Protein (APP). An altered proteolytic processing of APP implies that several biochemical processes (known and unknown) must take place in a highly complex ordered form, perhaps way beyond our abstraction capacity.
Many molecular lesions have been detected in Alzheimer´s disease, seems as accumulation of misfolded proteins in the aging brain results in oxidative and inflammatory damage, which in turn leads to energy failure and synaptic dysfunction. Brain cells are highly energy dependent for maintaining ion homeostasis during high metabolic activity [
7]. Decreasing brain metabolism (from Greek metabolikós: changeable, metabole: change, metaballein, to change) is a significant cause of cognitive abnormalities of AD.
Synapses are the first to show pathological variations in AD before the onset of clinical symptoms, because synaptic function has high energy demands. There is an age-related decline in neuronal NADH. Due to energy low levels, neuronal susceptibility to damage as a function of age and age related disease becomes important. In rat neuron model, mitochondria tend to be chronically depolarized, thereby producing more reactive oxygen species with age.
The already described pathogenic pathways leading to neurodegeneration in AD include accumulation of aberrant or misfolded proteins, ubiquitin-proteasome system dysfunction, excitotoxic reactions, oxidative and nitrosative stress, mitochondrial injury synaptic failure, altered metal homeostasis, dysfunction of axonal and dendritic transport [
8].
The major obstacle in managing the disease and designing rational therapeutic targets is our incomplete understanding of the pathogenesis of the disease. Several hypotheses have been proposed in an attempt to explain AD pathogenesis, including: amyloid deposition, tau phosphorylation, oxidative stress, metal ion dysregulation, and inflammation. No single one of these theories is sufficient to explain the spectrum of abnormalities found in the disease. However, the long-awaited answer about the fundamental initiator of the pathophysiological cascade in AD come to an end with the unraveling of the intrinsic property of melanin to split and re-form the water molecule.
If the available intracellular free chemical energy of the neuronal tissue is not sufficient for their incessant metabolic needs, sooner or later the affected organ or system become disorganized by a generalized failure being the hallmark of multifactorial disease. Brain energy metabolism is mainly centered in neuronal energy metabolism; however, other brain cells such as glial and vascular endothelial cells play an active role in the flux of biomass substrates to neurons. Recall that the basal rate of glucose utilization in astrocytes is higher than in neurons [
9-
11]. Glucose is the primary substrate for the buildup of biomass in brain tissue. By other side, energy is taken from the water of CSF.
Mitochondria are positioned within axons, dendrites, and synaptic terminals [
12] to keep low phosphates levels through ATP synthesis and also serve as calcium buffering for these compartments. Synaptic compartments are regions of neurons exposed to highest levels of oxidative and metabolic stress, thereby in presence of low levels of the best antioxidant: the molecular hydrogen, synapses are the sites where the neurodegenerative process occurs early in AD.
Water as Source of Energy
The dissociation of the water molecule can be schematized as follows:
2H2O ↔ 2H2 + O2 + 4e-
This reaction was termed Solis-Herrera cycle by its discoverer. When the water molecule is broken, then oxygen and hydrogen diatomic is released; but the most valuable reaction product is diatomic or molecular hydrogen due to be the energy carrier by excellence in the entire universe. By other hand, molecular oxygen, one of the most stable molecules already known, is toxic at any level. The dissociation of the water molecule is very expensive from energetic point of view, since in the laboratory the same process requires heat up the water until 2000°C.
Besides to be the energy carrier by excellence, diatomic hydrogen has other very valuable characteristic: it´s the best antioxidant; for instance is able to reduce the oxygen itself, forming water producing at the same time 4 high energy electrons for each two water molecules re-formed.
At least he's physically active and staying busy. But he was an intelligent guy spending time on books and stuff, still had a job and social interaction, was physically active, but even then he succumbed to Alzheimer's. There are some fates you just can't escape.
but because its weed, no drug will be developed
