February 07, 2013

Amyloid Plaques, B Vitamins and Oxidative Stress:

Amyloid Plaques and Alzheimer’s Disease:

Amyloid plaques are a characteristic brain feature in Alzheimer’s Disease.
They originate from a protein called APP.  If APP is broken down incorrectly the resulting protein can clump together into harmful plaques.

A rusty Pin:

An enzyme called Pin1 prevents this from happening.  But oxidative stress (a process similar to rusting!) impairs Pin1 activity, leading to increased plaque formation.

The role of vitamin B12 and folic acid:

Impaired methylation, due to low vitamin B12 and folic acid, also contributes toward plaque formation.  Two of the enzymes involved in plaque formation are kept in check by methylation of their genes.  In fact, one of these genes (PS1) is a known genetic risk factor for Alzheimer’s Disease.

Depriving cells of folic acid and vitamin B12 reduces SAM levels, impairs methylation and increases expression of these genes. This increases amyloid protein production.  Conversely, correcting this imbalance restores normal gene expression (Mol.Cell.Neurosci. 2005:28;195-04).  Similarly, in a ‘mouse model’ of the disease, folic acid deficiency increases expression of the two enzymes involved in plaque formation (J.Neurochem.2007:102;753-60).

The chicken and the egg:

The most recent scientific view is that a harmful cascade of events likely exists. This is because amyloid plaque formation causes oxidative stress. This then causes B vitamin depletion, raised homocysteine and impaired methylation. The result? Yet more amyloid formation - the harmful cycle repeats itself.

A breakable cycle:

Scientists suggest that such vicious cycles are breakable by diet or by supplements to increase the availability of folate and SAM (J. Alzheimer’s Disease. 2013: 33;1097-1094).  The ingredients in Betrinac uniquely address both impaired methylation and oxidative stress.

In our next blog update we will look at further ways in which homocysteine is harmful for your brain.

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