On February 4, 2008, Francesco Fornai* published the results of his test of Lithium on a small group of ALS patients in Italy with the results that Lithium delays progression. He and his colleagues found “. . .daily doses of lithium, leading to plasma levels ranging from 0.4 to 0.8 mEq/liter, delay disease progression in human patients affected by ALS. . .”
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Lithium as a Mood Stabilizer
Lithium has been prescribed for nearly three decades as a mood stabilizer although the precise mechanism is currently unknown. Recent research suggests three different mechanisms may act together to deliver the mood-stabilizing effect. An increasing number of scientists have come to the conclusion that the excitatory neurotransmitter glutamate is the key factor in understanding how lithium works. Other mood stabilizers such as valproate and lamotrigine exert influence over glutamate, suggesting a possible biological explanation for mania.
The other mechanisms by which lithium might help to regulate mood include the alteration of gene expression and the non-competitive inhibition of an enzyme called inositol monophosphatase.
Lithium for ALS
Here are the ALS treatment targets that Lithium appears to overlay biochemically. The results are noteworthy for the many possible connections. Most of these targets have been shown to possibly, probably or definitely help stem ALS progression and low-dosage Lithium appears to have excellent potential when correlated with published research. Low-dosage lithium has more connections to suspected targets for ALS than virtually any other medication for symptom treatment other than (possibly) BNG.