Transcranial Infrared Laser Stimulation Improves Cognition in Older Bipolar Patients: Proof of Concept Study

WHOM do we talk to to get this tested in stroke patients? With NO STROKE LEADERSHIP nothing will occur.  Augmenting prefrontal oxygenation sounds very likely to help stroke survivors.

Transcranial Infrared Laser Stimulation Improves Cognition in Older Bipolar Patients: Proof of Concept Study

 

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Courtney M. O’Donnell, PhD, Douglas W. Barrett, PhD, Latham H. Fink, MD, PhD,

First Published February 2, 2021 Research Article 

https://doi.org/10.1177/0891988720988906

Article information

Abstract

This is the first study to examine if transcranial infrared laser stimulation (TILS) improves cognition in older euthymic bipolar patients, who exhibit greater cognitive decline than is expected for age-matched controls. TILS is a non-invasive novel form of photobiomodulation that augments prefrontal oxygenation and improves cognition in young adults by upregulating the mitochondrial respiratory enzyme cytochrome-c-oxidase. We used a crossover sham-controlled design to examine if TILS to bilateral prefrontal cortex produces beneficial effects on cognition in 5 euthymic bipolar patients (ages 60-85). We measured cognitive flexibility, verbal fluency, working memory, sustained attention and impulsivity with tasks that have been shown to differentiate between healthy older adults and older bipolar adults. We found TILS-induced improvements in cognitive performance on the tasks that measure cognitive flexibility and impulsivity, after 5 weekly sessions of TILS. We concluded that TILS appeared both safe and effective in helping alleviate the accelerated cognitive decline present in older bipolar patients.

Keywords bipolar disorder, cognitive decline, brain stimulation, photobiomodulation, prefrontal cortex

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Maybe mine isn't high enough to have these problems. There is something to be said for being stroke-addled. I managed not getting straight A's in school so maybe I'm cool with not being bipolar.

Does High IQ Increase the Risk of Depression and Mental Disorders?

Enhancement of hippocampal neurogenesis by lithium

This is in rodents so don't start bugging your doctor that you need lithium. Unless maybe you are already taking this for bipolar or Schizophrenia.
http://www.ncbi.nlm.nih.gov/pubmed/10987856 

Chen G¹, Rajkowska G, Du F, Seraji-Bozorgzad N, Manji HK.

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Abstract

Increasing evidence suggests that mood disorders are associated with a reduction in regional CNS volume and neuronal and glial cell atrophy or loss. Lithium, a mainstay in the treatment of mood disorders, has recently been demonstrated to robustly increase the levels of the cytoprotective B-cell lymphoma protein-2 (bcl-2) in areas of rodent brain and in cultured cells. In view of bcl-2's antiapoptotic and neurotrophic effects, the present study was undertaken to determine if lithium affects neurogenesis in the adult rodent hippocampus. Mice were chronically treated with lithium, and 5-bromo-2-deoxyuridine (BrdU) labeling of dividing cells was conducted over 12 days. Immunohistochemical analysis was undertaken 1 day after the last injection, and three-dimensional stereological cell counting revealed that lithium produced a significant 25% increase in the BrdU-labeled cells in the dentate gyrus. Double-labeling immunofluorescence studies were undertaken to co-localize BrdU-positive cells with neuron-specific nuclear protein and showed that approximately 65% of the cells were double-labeled. These results add to the growing body of evidence suggesting that mood stabilizers and antidepressants exert neurotrophic effects and may therefore be of use in the long-term treatment of other neuropsychiatric disorders.

GSK-3 and Wnt Signaling in Neurogenesis and Bipolar Disorder

I would hope that all this stuff is being incorporated into some textbook. 

GSK-3 and Wnt Signaling in Neurogenesis and Bipolar Disorder

The canonical Wnt signaling pathway is critical for development of the mammalian central nervous system and regulates diverse processes throughout adulthood, including adult neurogenesis. Glycogen synthase kinase-3 (GSK-3) antagonizes the canonical Wnt pathway and therefore also plays a central role in neural development and adult neurogenesis. Lithium, the first line of therapy for bipolar disorder, inhibits GSK-3, activates Wnt signaling and stimulates adult neurogenesis, which may be important for its therapeutic effects. GSK-3 also regulates other critical signaling pathways which may contribute to the therapeutic effects of lithium, including growth factor/neurotrophin signaling downstream of Akt. Here we will review the roles of GSK-3 in CNS development and adult neurogenesis, with a focus on the canonical Wnt pathway. We will also discuss the validation of GSK-3 as the relevant target of lithium and the mechanisms downstream of GSK-3 that influence mammalian behavior.

Is Lithium a Potential Aid in Traumatic Brain Injury?

I'm not sure I would want to try this one. 

Is Lithium a Potential Aid in Traumatic Brain Injury?

Lithium carbonate serves as a primary treatment option in the treatment of mania and bipolar affective disorder. An elemental metal, lithium has atomic number 3 in the periodic table of elements.

The mechanism of action for lithium carbonate in bipolar disorder is unclear. Some of the proposed mechanisms for lithium in the central nervous system include:

• alteration of the neurotransmitter glutamate (affected by other drugs linked to therapeutic effect in bipolar disorder, i.e. sodium valproate and lamotrigine)
• alteration in gene expression
• inactivation of the GSK-3B (glycogen synthase kinase) enzyme known to be involved in circadian clock regulation
• interaction with the NO (nitrous oxide) signalling pathway

Inhibition of the GSK-3B enzyme has been shown to have potential beneficial effects in stimulating neuroplasticity as it is associated with enhanced expression of brain-derived neurotrophic factor (BDNF). Fengshan Yu and colleagues at NIH and the University of Health Sciences have recently explored the effect of lithium on traumatic brain injury using a mouse model.

In their experiment, mice received doses of lithium chloride ranging form 1.0 to 5.0 mEq/kg dose of lithium or placebo following a controlled episode of brain trauma under anesthesia. Doses were repeated daily for three days.

Brain injury response to lithium treatment was monitoring using neuropathological techniques as well as behavior and motor coordination tests. The key results of the study include:

• Lithium chloride at 1.5 to 3.0 mEq/kg reduced brain lesion volume compared to control
• Lithium chloride reduced post-trauma related anxiety behavior during the outcome monitoring
• Lithium chloride reduced breakdown of the blood-brain barrior
• Short-term and long-term motor coordination was better in the lithium group

The authors note that their study suggests the neuroprotective effect of lithium administration following traumatic brain injury in the mouse model appears related to a GSK-3B mechanism. The study timed lithium administration to 3 hours after the trauma providing a realistic model for a trial in human clinical scenarios. They conclude "Our results that demonstrate its (lithium chloride) benefits in the mouse model pave the way for early clinical trials as potential treatment for TBI (traumatic brain injury) patients.