The largest cause of disability

This BMJ report caught my eye because of the amount research interest there is in LLLT for brain pathologies (see bottom of this article for list)

BMJ report: Mental illness is the single largest cause of disability in the UK

It contributes up to 22.8% of the total cost burden compared with 15.9% for cancer and 16.2% for cardiovascular disease

One third of the adult population suffers a mental disorder every year. Brain disorders cost the world more that any other disease and yet distribution of medical research funding in the UK is as follows

13% Cancer
7% Coronary heart disease
1% Stroke
0.5% Dementia

Researchers conducted a systematic review of UK and European studies on the prevalence and economic burden of brain disorders. They found that there were 45 million cases of neurological and psychiatric diseases in the United Kingdom, which cost £112bn in healthcare, social care, and indirect costs.

Dementia alone had an annual cost of £18.6bn, compared to £12bn for cancer and £8bn for coronary heart disease. Other brain disorders in the UK with a substantial economic burden included mood disorders (£16.1bn), psychotic disorders (£14bn), anxiety disorders (£9.8bn), and stroke (£7.3bn). The costs were calculated for 2010, the most recent year for which data are available, and the authors are confident that their estimate is conservative.

Approximately 46% of the overall cost of brain disorders was due to productivity losses (£52.3bn). The remaining costs were due to direct healthcare costs (£30.2bn) and direct non-medical costs (£30.3bn), such as social services, informal care and special accommodation.

The study also noted that mental illness was the “single largest cause of disability in the UK, contributing up to 22.8% of the total burden, compared with 15.9% for cancer and 16.2% for cardiovascular disease.”

http://www.bmj.com/content/347/bmj.f4766?etoc=

Shining light on the brain for functional and cognitive problems is an extremely promising area of LLLT research 

Here is a crude (unfiltered) list of LLLT / brain related research

http://www.ncbi.nlm.nih.gov/pubmed/?term=(LLLT+TBI)+OR+(LLLT+stroke)+OR+(LLLT+Alzheimers)+OR+(LLLT+PTSD)+OR+(LLLT+TBI)+OR+(TLT+stroke)+OR+(TLT+Alzheimers)+OR+(TLT+PTSD)+OR+(LLLT+dementia)

here is one I collaborated on  

Low-Level Laser Light Therapy Improves Cognitive Deficits and Inhibits Microglial Activation after Controlled Cortical Impact in Mice.

Khuman J, Zhang J, Park J, Carroll J, Whalen M

Massachusetts General Hospital , Neuroscience Center and Department of Pediatrics, 149 Thirteenth street, Charlestown, Massachusetts, United States, 02129; 

Low-level laser light therapy (LLLT) exerts beneficial effects on motor and histopathological outcome after experimental TBI (Oron et al., 2007), and coherent near infrared light has been reported to improve cognitive function in patients with chronic TBI (Naeser et al., 2010). However, effects of LLLT on cognitive recovery in experimental TBI are lacking. We hypothesized that LLLT administered after controlled cortical impact (CCI) would improve postinjury Morris water maze performance. Low-level laser light (800 nm) was applied directly to the contused parenchyma or transcranially in mice beginning 60-80 min after CCI. Injured mice treated with 60 J/cm2 (500 mW/cm2 x 2 min) either transcranially or via an open craniotomy had modestly improved latency to the hidden platform (p < 0.05 for group) and probe trial performance (p < 0.01) compared to non-treated controls. The beneficial effects of LLLT in open craniotomy mice were associated with reduced microgliosis at 48h (21.8 + 2.3 vs. 39.2 + 4.2 IbA-1+ cells/x200 field, p < 0.05). Little or no effect of LLLT on postinjury cognitive function was observed using other doses, a 4 h administration time point and 7 day administration of 60 J/cm2. No effect of LLLT (60 J/cm2 open craniotomy) was observed on postinjury motor function (d 1-7), brain edema (24 h), nitrosative stress (24 h), or lesion volume (14 d). Although further dose optimization and mechanism studies are needed, the data suggest that LLLT might be a therapeutic option to improve cognitive recovery and limit inflammation after TBI.

J Neurotrauma 2011 Aug 18

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=21851183

since then we have performed  more studies giving us more dose data

below are three lab studies specifically looking Alzheimer’s markers 

Transcranial Laser Therapy Attenuates Amyloid-beta Peptide Neuropathology in Amyloid-beta Protein Precursor Transgenic Mice.

Taboada LD, Yu J, El-Amouri S, Gattoni-Celli S, Richieri S, McCarthy T, Streeter J, Kindy MS

PhotoThera, Inc., Carlsbad, CA. USA

Transcranial laser therapy (TLT) was tested for efficacy in a mouse model of Alzheimer’s disease (AD) using a near-infrared energy laser system. TLT is thought to stimulate ATP production, increase mitochondrial activity, and help maintain neuronal function. Studies were performed to determine the effect of TLT in an amyloid-beta protein precursor (AbetaPP) transgenic mouse model. TLT was administered 3 times/week at various doses, starting at 3 months of age, and was compared to a control group (no laser treatment). Treatment was continued for a total of six months. Animals were examined for amyloid load, inflammatory markers, brain amyloid-beta (Abeta) levels, plasma Abeta levels, cerebrospinal fluid Abeta levels, soluble AbetaPP (sAbetaPP) levels, and behavioral changes. The numbers of Abeta plaques were significantly reduced in the brain with administration of TLT in a dose-dependent fashion. Administration of TLT was associated with a dose-dependent reduction in amyloid load. All TLT doses mitigated the behavioral effects seen with advanced amyloid deposition and reduce the expression of inflammatory markers in the AbetaPP transgenic mice. All TLT doses produced an increase in sAbetaPPalpha and a decrease in CTFbeta levels consistent with inhibition of the beta-secretase activity. In addition, TLT showed an increase in ATP levels, mitochondrial function, and c-fos suggesting an overall improvement in neurological function. These studies suggest that TLT is a potential candidate for treatment of AD.

J Alzheimers Dis 2010 Nov 29

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=21116053

Low energy laser light (632.8 nm) suppresses amyloid-beta peptide-induced oxidative and inflammatory responses in astrocytes.

Yang X, Askarova S, Sheng W, Chen JK, Sun AY, Sun GY, Yao G, Lee JC

Department of Biological Engineering, University of Missouri, Columbia, MO 65211, USA.

Oxidative stress and inflammation are important processes in the progression of Alzheimer’s disease (AD). Recent studies have implicated the role of amyloid beta-peptides (Abeta) in mediating these processes. In astrocytes, oligomeric Abeta induces the assembly of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase complexes resulting in its activation to produce anionic superoxide. Abeta also promotes production of pro-inflammatory factors in astrocytes. Since low energy laser has previously been reported to attenuate oxidative stress and inflammation in biological systems, the objective of this study was to examine whether this type of laser light was able to abrogate the oxidative and inflammatory responses induced by Abeta. Primary rat astrocytes were exposed to Helium-Neon laser (lambda=632.8 nm), followed by the treatment with oligomeric Abeta. Primary rat astrocytes were used to measure Abeta-induced production of superoxide anions using fluorescence microscopy of dihydroethidium (DHE), assembly of NADPH oxidase subunits by the colocalization between the cytosolic p47(phox) subunit and the membrane gp91(phox) subunit using fluorescent confocal microscopy, phosphorylation of cytosolic phospholipase A(2) cPLA(2) and expressions of pro-inflammatory factors including interleukin-1beta (IL-1beta) and inducible nitric-oxide synthase (iNOS) using Western blot Analysis. Our data showed that laser light at 632.8 nm suppressed Abeta-induced superoxide production, colocalization between NADPH oxidase gp91(phox) and p47(phox) subunits, phosphorylation of cPLA(2,) and the expressions of IL-1beta and iNOS in primary astrocytes. We demonstrated for the first time that 632.8 nm laser was capable of suppressing cellular pathways of oxidative stress and inflammatory responses critical in the pathogenesis in AD. This study should prove to provide the groundwork for further investigations for the potential use of laser therapy as a treatment for AD.

Neuroscience 2010 Sep 25

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=20884337

670 nm Laser Light and EGCG Complementarily Reduce Amyloid-beta Aggregates in Human Neuroblastoma Cells: Basis for Treatment of Alzheimer’s Disease?

Sommer AP, Bieschke J, Friedrich RP, Zhu D, Wanker EE, Fecht HJ, Mereles D, Hunstein W

1 Institute of Micro and Nanomaterials, Nanobionic Laboratory, University of Ulm , Ulm, Germany .

Abstract  Objective: The aim of the present study is to present the results of in vitro experiments with possible relevance in the treatment of Alzheimer’s disease (AD). Background Data: Despite intensive research efforts, there is no treatment for AD. One root cause of AD is the extra- and intracellular deposition of amyloid-beta (Abeta) fibrils in the brain. Recently, it was shown that extracellular Abeta can enter brain cells, resulting in neurotoxicity. Methods: After internalization of Abeta(42) into human neuroblastoma (SH-EP) cells, they were irradiated with moderately intense 670-nm laser light (1000 Wm(-2)) and/or treated with epigallocatechin gallate (EGCG). Results: In irradiated cells, Abeta(42) aggregate amounts were significantly lower than in nonirradiated cells. Likewise, in EGCG-treated cells, Abeta(42) aggregate amounts were significantly lower than in non-EGCG-treated cells. Except for the cells simultaneously laden with Abeta(42) and EGCG, there was a significant increase in cell numbers in response to laser irradiation. EGCG alone had no effect on cell proliferation. Laser irradiation significantly increased ATP levels in Abeta(42)-free cells, when compared to nonirradiated cells. Laser-induced clearance of Abeta(42) aggregates occurred at the expense of cellular ATP. Conclusions: Irradiation with moderate levels of 670-nm light and EGCG supplementation complementarily reduces Abeta aggregates in SH-EP cells. Transcranial penetration of moderate levels of red to near-infrared (NIR) light has already been amply exploited in the treatment of patients with acute stroke; the blood-brain barrier (BBB) penetration of EGCG has been demonstrated in animals. We hope that our approach will inspire a practical therapy for AD.

Photomed Laser Surg 2011 Oct 26

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=22029866

 this is a different kind of pathology but shows its use in anxiety and depression 

 Psychological benefits 2 and 4 weeks after a single treatment with near infrared light to the forehead: a pilot study of 10 patients with major depression and anxiety.

Schiffer F, Johnston AL, Ravichandran C, Polcari A, Teicher MH, Webb RH, Hamblin MR

The Department of Psychiatry, Harvard Medical School and the Developmental Biopsychiatry Research Program, McLean Hospital, 115 Mill Street Belmont, MA 02478 USA. fschiffer@mclean.harvard.edu.

ABSTRACT: BACKGROUND: Many studies have reported beneficial effects from the application of near-infrared (NIR) light photobiomodulation (PBM) to the body, and one group has reported beneficial effects applying it to the brain in stroke patients. We have reported that the measurement of a patient’s left and right hemispheric emotional valence (HEV) may clarify data and guide lateralized treatments. We sought to test whether a NIR treatment could 1. improve the psychological status of patients, 2. show a relationship between immediate psychological improvements when HEV was taken into account, and 3. show an increase in frontal pole regional cerebral blood flow (rCBF), and 4. be applied without side effects. METHODS: We gave 10 patients, (5 M/5 F) with major depression, including 9 with anxiety, 7 with a past history of substance abuse (6 with an opiate abuse and 1 with an alcohol abuse history), and 3 with post traumatic stress disorder, a baseline standard diagnostic interview, a Hamilton Depression Rating Scale (HAM-D), a Hamilton Anxiety Rating Scale (HAM-A), and a Positive and Negative Affect Scale (PANAS). We then gave four 4-minute treatments in a random order: NIR to left forehead at F3, to right forehead at F4, and placebo treatments (light off) at the same sites. Immediately following each treatment we repeated the PANAS, and at 2-weeks and at 4-weeks post treatment we repeated all 3 rating scales. During all treatments we recorded total hemoglobin (cHb), as a measure of rCBF with a commercial NIR spectroscopy device over the left and the right frontal poles of the brain. RESULTS: At 2-weeks post treatment 6 of 10 patients had a remission (a score </= 10) on the HAM-D and 7 of 10 achieved this on the HAM-A. Patients experienced highly significant reductions in both HAM-D and HAM-A scores following treatment, with the greatest reductions occurring at 2 weeks. Mean rCBF across hemispheres increased from 0.011 units in the off condition to 0.043 units in the on condition, for a difference of 0.032 (95% CI: -0.016, 0.080) units, though this result did not reach statistical significance. Immediately after treatment the PANAS improved to a significantly greater extent with NIR “on” relative to NIR “off” when a hemisphere with more positive HEV was treated than when one with more negative HEV was treated. We observed no side effects. CONCLUSION: This small feasibility study suggests that NIR-PBM may have utility for the treatment of depression and other psychiatric disorders and that double blind randomized placebo-controlled trials are indicated. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT00961454.

Behav Brain Funct 2009 5 46

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=19995444

 

About James Carroll

Founder and CEO at THOR Photomedicine Ltd. About THOR
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