Cerebral Atrophy

Cerebral atrophy is a common feature of the many neurodegenerative diseases that affect the brain. Atrophy of any tissue means loss of cells. In brain tissue, atrophy describes a loss of neurons and the connections between them. Atrophy can be generalized, which means that all of the brain have shrunk; or it can be focal, affecting only a limited area of brain and resulting in a decrease of functions of that area of the brain controls. If the cerebral hemispheres (the two lobes of the brain that form cerebrum) are affected, conscious thought and voluntary processes may be impaired.

Neurodegenerative diseases is a condition which affects brain function. Neurodegenerative diseases result from deterioration of neurons.

List of neurodegenerative diseases

• Alzheimer
• Amyotrophic lateral sclerosis
• Ataxia telangiectasia
• Batten disease (also known as Spielmeyer-Vogt-Sjogren-Batten disease)
• Canavan disease
• Cockayne syndrome
• Corticobasal degeneration
• Creutzfeldt-Jakob disease
• Huntington disease
• Kennedy’s disease
• Krabbe disease
• Lewy body dementia
• Machado-Joseph disease (Spinocerebellar ataxia type3)
• Multiple sclerosis
• Multiple System Atrophy
• Parkinson disease
• Pelizaeus-Merzbacher Disease
• Pick’s disease
• Primary lateral sclerosis
• Refsum’s disease
• Sandhoff disease
• Schilder’s disease
• Spinocerebellar ataxia (multiple types with varying characteristics)
• Spinal muscular atrophy
• Steele-Richardson-Olszewski disease
• Tabes dorsalis

Free Radicals and Oxidative Stress in Neurodegenerative Diseases

Neurodegenerative diseases: An overview

Neurodegenerative disorders are a heterogeneous group of diseases of nervous system, including the brain, spinal cord, and peripheral nerves, that have many different aetiologies. Many are hereditary, some are secondary to toxic or metabolic processes and others result from infections. Neuropathologically, these are characterised by abnormalities of relatively specific regions of brain and specific populations of neurons. The degenerating neuron clusters in different diseases determine clinical phenotype of that particular illness.

Free radicals

Free radicals are highly reactive molecules or chemical species capable of independent existence. Generation of highly Reactive Oxygen Species (ROS) is an integral feature of normal cellular function like mitochondrial respiratory chain, phagocytosis, arachidonic acid metabolism, ovulation and fertilisation. Their production however, multiplies several folds during pathological conditions.

Oxygen, because of its bi-radical nature, readily accepts unpaired electrons to give rise to a series of partially reduced species collectively known as ROS (Reactive Oxygen Species). Damage due to free radicals caused by ROS leads to several damaging effects as they attack lipids, protein/ enzymes, carbohydrates and DNA in cells and tissues. They induce undesirable oxidation, causing membrane damage, protein modification, DNA damage, and cell death induced by DNA fragmentation and lipid peroxidation.

Antioxidant systems

Endogenous antioxidants :

Biological systems have evolved with endogenous defense mechanisms to help protect against free radical induced cell damage. Glutathione peroxidase, catalase and superoxide dismutases are antioxidant enzymes, which metabolize toxic oxidative intermediates. They require micronutrient as cofactors like selenium, iron, copper, zinc and manganese for optimum catalytic activity and effective antioxidant defense mechanisms. Glutathione, ascorbic acid, alpha-tocopherol, betacarotene, bilirubin, selenium, NADPH, butylhydroxyanisole (BHA), mannitol, benzoate, histidine peptide, the iron-bonding transferrin, dihydrolipoic acid, reduced CoQ10, melatonin, uric acid and plasma protein and thiol, as a whole play a homoeostatic or protective role against ROS produced during normal cellular metabolism and after active oxidation insult.

Exogenous antioxidants :

The most widely studied dietary antioxidants are vitamin C, vitamin E, and beta-carotene. Vitamin C is the most important water-soluble antioxidant in extracellular fluids, as it is capable of neutralising ROS in aqueous phase before lipid peroxidation is initiated. Vitamin E is a major lipid-soluble antioxidant and is the most effective chain-breaking antioxidant within the cell membrane where it protects membrane fatty acids from lipid peroxidation. Beta-carotene and other carotenoids also provide antioxidant protection to lipid rich tissues.

A number of other dietary antioxidants exist beyond the traditional vitamins collectively known as phytonutrients or phytochemicals which are being increasingly appreciated for their antioxidant activity, one example is flavonoids which are a group of polyphenolic compounds

Oxidative stress in the nervous system

The nervous system including brain, spinal cord and peripheral nerves is rich in both unsaturated fatty acids and iron. The high lipid content of nervous tissue, coupled with its high aerobic metabolic activity, makes it particularly susceptible to oxidative damage. The high level of iron may be essential, particularly during brain development, but its presence also means that injury to brain cells may release iron ions, which lead to oxidative stress via the iron-catalysed formation of ROS. In addition, those brain regions that are rich in catecholamines are exceptionally vulnerable to free radical generation. The catecholamine adrenaline, noradrenaline and dopamine can spontaneously break down (auto-oxidise) to free radicals or can be metabolized to radicals by endogenous enzymes such as MAO (monoamine oxidases).

A number of in vitro studies showned that antioxidants – both endogenous and dietary – protect nervous tissue from damage by oxidative stress. Vitamin E prevented cell death (apoptosis) in rat neurons subjected to hypoxia followed by oxygen reperfusion. In the same study, it was shown that vitamin E prevented neuronal damage from reactive nitrogen species. Both vitamin E and beta carotene protected rat neurons against oxidative stress from exposure to ethanol. In an experimental model of diabetes-caused neurovascular dysfunction, beta-carotene protected cells most effectively followed by vitamins E and C.

There is substantial evidence that oxidative stress is a causative or at least ancillary factor in the pathogenesis of major neurodegenerative diseases, including Parkinson’s disease, Alzheimer’s disease and amyotrophic lateral sclerosis (ALS, “Lou Gehrig’s disease”) as well as in cases of stroke, trauma and seizures. Decreased levels of antioxidant enzyme activity are reported in patients with Parkinson’s disease. Evidence of increase in lipid peroxidation and oxidation of DNA and proteins has indeed been seen substantia nigra of patients affected with Parkinson’s disease. Similar increase in markers of oxidative stress was also seen in Alzheimer’s disease, Huntington’s disease and in both familial ALS (FALS) and sporadic ALS (SALS) patients.

The role of free-radical-mediated oxidative injury in acute insults to nervous system including stroke or trauma and in chronic neurodegenerative disorders, is being just recognised. As we know, oxygen is an essential molecule for survival of majority of living organisms. Oxidative stress is the harmful condition that occurs when there is excess free radicals and/or a decrease in antioxidant levels. There is evidence to suggest that increase in energy metabolism by aerobic pathways enhances intracellular concentration of free oxygen radicals, which in turn enhance rate of autocatalytic process of lipid peroxidation, inducing damage to brain structures, especially when physiological defences become insufficient or depleted. Antioxidants combat oxidative stress by working to neutralise excess free radicals and stopping them from starting chain reactions that contribute to various diseases and premature aging. Evidence to date for oxidative stress in PD, TD, SCZ, AD and other neurodegenerative diseases are strongly persuasive. Clinical studies show that a number of events associated with Alzheimer’s are capable of stimulating production of free radicals and depletion of antioxidant levels. Patients with Parkinson’s also have reduced glutathione levels and free radical damage is found in the form of increased lipid peroxidation and oxidation of DNA bases.

Role of Noni

NONI works as powerful antioxidants

Noni has the most powerful antioxidant properties. It helps a lot to protect our vital organs including brain from the deadly attack of free radicals. Noni contains all the vitamins, rich in beta-carotenes, abundant source of trace minerals, flavonoids, besides that more than 150 + most beneficial micronutrients.

Antioxidant property of NONI can fight free radicals in three ways.

1. It prevents a free radical from forming.

2. It interrupts an oxidizing chain reaction to lessen effects of free radicals.

3. Antioxidant like Noni reduces the free radical’s impact.

Noni as an antioxidant helps neutralize effects of free radicals, allowing the body to restore itself to proper balance leading to health and well-being. Noni contains many different synergistic antioxidant nutrients, including basic vitamins A,C & E. Drinking Noni every day helps combat the damaging effects of free radicals.

The natural integrity of Noni is only part of the reason for its effectiveness. There are two additional reasons contributing to NONI’s effectiveness for a broad range of conditions

Unique Combinations of Substances

Synergy of its Substances 

Noni plays a vital role in preventing and also to some extent therapeutic point of view to many neurodegenerative diseases where cerebral atrophy is just a common feature.

Recommended Dosage

Divine Noni Concentrate

5ml morning and 5ml evening for 3 days. Then

10ml morning and 10ml evening for next 3 days. Then

15ml morning and 15ml evening for next 15 days. Then

20ml morning and 20ml evening for next 8 months.