Does lithium prevent Alzheimer's disease?

Does lithium prevent Alzheimer's disease?
https://www.ncbi.nlm.nih.gov/pubmed/22500970
Abstract

Lithium salts have a well-established role in the treatment of major affective disorders. More recently, experimental and clinical studies have provided evidence that lithium may also exert neuroprotective effects. In animal and cell culture models, lithium has been shown to increase neuronal viability through a combination of mechanisms that includes the inhibition of apoptosis, regulation of autophagy, increased mitochondrial function, and synthesis of neurotrophic factors. In humans, lithium treatment has been associated with humoral and structural evidence of neuroprotection, such as increased expression of anti-apoptotic genes, inhibition of cellular oxidative stress, synthesis of brain-derived neurotrophic factor (BDNF), cortical thickening, increased grey matter density, and hippocampal enlargement. Recent studies addressing the inhibition of glycogen synthase kinase-3 beta (GSK3B) by lithium have further suggested the modification of biological cascades that pertain to the pathophysiology of Alzheimer's disease (AD). A recent placebo-controlled clinical trial in patients with amnestic mild cognitive impairment (MCI) showed that long-term lithium treatment may actually slow the progression of cognitive and functional deficits, and also attenuate Tau hyperphosphorylation in the MCI-AD continuum. Therefore, lithium treatment may yield disease-modifying effects in AD, both by the specific modification of its pathophysiology via inhibition of overactive GSK3B, and by the unspecific provision of neurotrophic and neuroprotective support. Although the clinical evidence available so far is promising, further experimentation and replication of the evidence in large scale clinical trials is still required to assess the benefit of lithium in the treatment or prevention of cognitive decline in the elderly.

Chronic Microdose Lithium Treatment Prevented Memory Loss and Neurohistopathological Changes in a Transgenic Mouse Model of Alzheimer's Disease
(complete study on the link)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4659557/

Introduction

Demographic changes resulting from the increase in life span and the increasing number of aged people lead to a dramatic increase in the prevalency of dementias. Among them, Alzheimer’s disease is a progressive neurodegenerative disease, whose ethiology is still unknown, and causes progressive cognitive deficit and incapacity. Aging is the most important risk factor, suggesting that biological alterations related to aging may be associated to its pathogenesis [1], besides genetic and environmental factors. Normally, patients present progressive atrophy of gray matter, which can be a reflection of neuronal death caused by micro-structural changes in brain [2].

Gradual accumulation of neurofibrillary tangles, mainly intracellularly, formed as a result of abnormal hyperphosphorylation of cytoskeletal tau protein and deposition of amyloid-β peptide fibrils into senile plaques, mainly extracellularly, are the most important histopathological characteristics of AD that lead to huge neuronal death [3]. The biochemical mechanisms that are activated to produce these alterations are many and are evidently present in specific vulnerable brain areas. One of the brain areas most succeptible is the hippocampus [4].

Recently, our research team showed that treatment with microdose lithium carbonate (1.5 mg/day) was efficient to prevent the cognitive decline of patients with clinical diagnosis for AD [5]. Although these exciting data in humans, there is no evidence of the efficacy of this microdose as a preventive strategy. In the same way, the ability to modify the disease properties was not measured yet. The neuroprotective mechanisms of lithium have already been described [6,7] and the benefits of lithium involve inhibition of GSK-3β leading to decreased tau phosphorylation and to the decrease of amyloid-β (Aβ) load [8,9]. Lithium may also protect neurons against the neurotoxic effects of Aβ42 by favoring other neurotrophic and/or neuroprotective responses not only by GSK3 inhibition. Another important neuroprotective effect of lithium is the stimulation of synthesis and release of neurotrophins, in particular brain-derived neurotrophic factor (BDNF) and vascular endothelial growth factor (VEGF) [7]. Therefore, lithium treatment may provide an array of benefits that could lead to a global improvement in the organism function.

However, it is already known that lithium could be toxic in weight-based dosing [10], mainly in aged people. So, the aim of this work was to investigate the preventive and therapeutic effects of microdose lithium in a mouse model of neurodegenerative disease and to explore their molecular mechanisms. This work is the first to show that continuous preventive, as well as continuous therapeutic treatment with microdose lithium can alter the pathological characteristics of Alzheimer’s disease, preventing its evolution. In this way, this work gives support for the clinical use of microdose lithium to prevent and stabilize the progression of the disease.

So many pro's and con's ...
But at least researchers are looking at different treatments.

I still think our genes/family history play a part.
With many families heart disease is prevalent, with others Alzheimer's...

All the best Jan

Interesting! A lot of "psychiatric" meds have negative effects on many other disease processes so it's nice to see one that may be beneficial for a change.

There will be very little research or interest since lithium is sold as a supplement in the USA. You can buy 5mg of elemental lithium as lithium oratate or lithium aspartate pretty cheap. Epidemiology studies find that places with higher lithium levels in water have less crime and better mortality rates. Dosages (in the hundreds) as used for mental treatments can be toxic long term. Micro dosages of 1.5 mg seem to have some benefits in humans.

Is a commercial site but has a nice compilation of lithium research with references;

REALLY Low Dose Lithium Stabilizes Alzheimer’s Disease Patient Cognition Over 15 Months

http://www.life-enhancement.com/magazine/article/3288-really-low-dose-lithium-stabilizes-alzheimers-disease-patient-cognition-over-15-months

Good grief, that's all news to me.

Lithium is in the same group of elements as sodium and potassium which are both vital, especially the balance between them.