A New Therapeutic Approach for Improving Dementia of the ALZHEIMER TYPE

RESULTS:
Results from all the patients who have been evaluated are given in Table I. In this table, each patient’s initial, sex, age result of the MMSE and the GDS before and after treatment as well as the improvement are listed.

The minimum improvement after NADH treatment was 1 point in three patients, the maximum 2 points in 14 patients. This yielded a mean value of 1.82. The duration of therapy lasted from a minimum of eight weeks to a maximum of 12 weeks, with a mean value of 9.65.

The statistical analysis of the results as listed in Table I, and the evaluations are given in Table II.

The age of the patients ranged from 33 to 84 years, with a mean value of 67.71 and a medium of 68. The MMSE before NADH treatment revealed a minimum value of 16 observed in one patient and a maximum value of 24 in six patients yielding a mean value of 15.82.

After treatment with NADH in the MMSE score a minimum value of 16 was observed in one patient, and a maximum score of 30 was found in six patients with a mean value of 24 ( ¹⁸ ). Considering the improvement after NADH treatment based on the MMSE, the minimum was 6 and the maximum 14 with a mean value of 8.35.

In addition to the MMSE, the GDS was used to examine the dementia patients.

The minimum in the GDS was 2 in one patient, the maximum 6 in six patients yielding a mean value of 4.29. After application of NADH, the minimum in the GDS rating was 1 in seven patients, the maximum 4 in seven patients. The mean value of all patients was 2.47.

All the patients examined by the MMSE and the global deterioration scale showed a distinct improvement after NADH therapy. This holds not only for patients with mild symptoms of cognitive decline (MMSE = 24 and GDS = 3) but also for patients with moderately severe or severe dementia (MMSE = 4-20, GDS = 5-6).

DISCUSSION:
Using NADH as therapeutic regimen for demented patients is based on the hypothesis that the stimulation of the endogenous biosynthesis of certain neurotransmitters, in particular dopamine and noradrenaline, should improve the mental performance of patients with cognitive dysfunction and/or dementia as these neurotransmitters are reduced in certain brain areas of Alzheimer patients ( ^{12, 13, 14} ).

As shown in in vitro studies using phaeochromocytoma cells, NADH increases the biosynthesis of dopamine up to sixfold ( ²⁶ ). Furthermore, it has been shown that NADH increases the level of dopamine in the striatum of the rat brain after peritoneal injection of NADH. These observations provide possible explanations for the mechanism of the action of NADH. From the studies with more than 800 patients with Parkinson disease, it was learned that the dopamine concentration increases in the serum after NADH treatment ( ²⁰ ). As the short term memory as well as certain other cognitive functions of Parkinsonian patients improved simultaneously, it was tempting to use NADH with patients suffering from dementia of the Alzheimer type. In a number of our patients, it was possible to measure dopamine and noradrenaline concentration in the plasma before and after treatment with NADH. Both of these neurotransmitters showed an increase after the NADH treatment period in these patients.

Furthermore, measurement was made of the enzyme NADH Ubiquinone reductase (Complex I of the respiratory chain) in platelets before and after treatment with NADH. Before therapy, the values of the enzymatic activity were between 30 and 60 percent lower than that of age matched controls. After NADH treatment, activity of Complex I increased. These preliminary findings indicate that NADH stimulates not only the endogenous biosynthesis of dopamine and noradrenaline, but also the energy production in the cells, at least in the platelets. Whether or not this positive effect on the cellular energy production is one of the molecular mechanisms by which NADH improves the dementious systems remains to be elucidated. However, it seems reasonable to assume that cells which have more energy available can perform processes more efficiently. They may also survive longer because the state of energy of the mitochondria does play a role in the life time of a cell. Cells injected with mitochondria from very young cells live longer than cells injected with mitochondria from older cells ( ²² ).

. . . continued on the next page