Why not use lithium for Alzheimer’s disease prevention and treatment? Good question. Studies indicate that lithium is a viable option for preventing and slowing the progression of Alzheimer’s disease.
Characteristics of Alzheimer’s Disease
Alzheimer’s disease is the sixth leading cause of death in the United States. Worldwide an estimated 36 million people have Alzheimer’s disease. This number will increase to 66 million by 2030 and triple by 2050.
A progressive course
Alzheimer’s is characterized by progressive shrinking of brain tissue. This neurological infirmity causes a cataclysmic plummet in memory and social skills that ultimately leads to death.
Less than 5% of the time Alzheimer’s disease results from genetic mutations on chromosomes 1, 14, and 21 that predict AD before age 60. More commonly a slow cumulative and complex pattern of lifestyle, environmental and muted genetic factors contribute to Alzheimer’s after the age of 65.
Pathology of Alzheimer’s
Alzheimer’s disease results from two distinctive features: plaques and tangles.
Plaques
Clumps of protein fragments called plaques block the spaces between brain cells. These beta-amyloid peptide plaques block the transmission of nerve cells. This barricade stops the communication between brain cells.
Neurofibrillary tangles
Meanwhile, disruption of the tau protein cause neurofibrillary tangles to develop inside the nerve cell. Healthy Tau protein filaments help circulate nutrients throughout the cell. In Alzheimer’s disease these filaments become twisted cutting off cell nutrition. The cells die. Memory is impaired, learning halted.
The aging brain
Moreover, evidence indicates that plaque and tangles appear relatively often in the aging brain. Plaques may appear three to four decades before symptoms of cognitive decline appear. One study found that 10% of 50-year olds; 33% of 80-year olds and 44% of 90-year olds had amyloid plaques. About a third of patients over 85-years of age have Alzheimer’s.
Traditional Treatments for Alzheimer’s Disease
Numerous research projects in the past two decades have found no medicine that effectively treats Alzheimer’s. The older medications continue to disappoint.. Cholinesterase inhibitors Aricept (donepezil), Razadyne (galantamine) and Exelon (rivastigmine) may, at best, marginally slow the progression of Alzheimer’s. The NMDA antagonist Namenda offers little improvement. The ketone enhancer Axona fails to stop the progression of the illness.
On the other hand, the MIND diet rich in whole grains, berries, leafy green vegetables, nuts and legumes lessen the risk for Alzheimer’s disease. In contrast, excessive sugar intake increases the risk of Alzheimer’s.
Furthermore exercise reduces the risk of Alzheimer’s. Irisin a messenger protein released by muscle cells in response to the contractions that occur during physical activity promotes brain health.
Traditional Uses for Lithium
Lithium, a well-established therapeutic option for the acute and long-term management of bipolar disorder, has been shown to be an effective augmentation medication in the treatment of depression. Lithium also has anti-suicidal effects. Lithium reduces the risk of suicide by 60% and the risk of self-harm by 70%.
In addition numerous studies have shown that lithium can be useful in the preventing and slowing the progression of Alzheimer’s disease.
Neuroprotective Effects of Lithium
Initially researchers became interested in the use of lithium for treating Alzheimer’s diseases when they observed that bipolar patients taking lithium therapy had lower rates of cognitive decline than those on other medications. Later, In a placebo controlled study of 232 patients lithium significantly decreased cognitive decline as compared to placebo.
In addition, studies have found that lithium can be effective for Alzheimer’s when used at low-doses similar to those found naturally in water. Studies show that the benefits lithium can be achieved with doses between 0.3 mg-5 mg. The lower the dose, the less side effects.
Furthermore, Lithium at both high and low concentrations have been shown to increase neuronal viability and resilience. Lithium inhibits Glycogen Synthase Kinase-3 (GSK-3), the enzyme responsible for the development of the amyloid plaques and neurofibrillary tangles associated with Alzheimer’s disease.
Moreover, Lithium increases the synthesis and release of Brain Derived Neurotrophic factor (BDNF) and neurotrophic (NT-3) that stimulate the growth and repair of neurons. Patients taking lithium have higher brain gray matter suggesting that lithium has powerful stimulatory effects on neurogenesis. One study showed that lithium increased the number and length of dendrites in damaged nerve cells.
Conclusion
After a careful and thorough review of the literature I have concluded that the benefits of low dose lithium in the treatment of cognitive decline and Alzheimer’s dementia far out-weight the risks of side effects. The earlier the treatment begins in the course of the illness the more effective the treatment. For my patients with early cognitive decline and early onset dementia I am going to recommend the MIND diet, 150 minutes of weekly exercise and lithium orotate 5 mg at bedtime.