Alzheimer's disease (AD) is a common, chronic expensive debilitating 
neurodegenerative disease with no current treatments to prevent the physical 
deterioration of the brain and the consequent cognitive deficits. The current 
pathophysiology of Alzheimer's disease is the accumulation of neurofibrillary 
tangles (NFTs) of hyperphosphorylated tau protein and amyloid-beta (Aβ) plaques. 
Antibody therapy of Tau and Amyloid beta, vaccines and other methods to decrease 
Tau and or Amyloid have not been successful after considerable pharmaceutical 
and biotech efforts. For example, Eli Lilly announced a major change to its 
closely watched clinical trial for the Alzheimer's drug solanezumab which failed 
to reach statistical significance. Recently, a report on animal models using 
photomodulation with near infrared light to treat AD pathology in K369I tau 
transgenic model (K3) l engineered to develop neurofibrillary tangles, and the 
APPs/PSEN1dE9 transgenic model (APP/PS1) to develop amyloid plaques. Mice were 
treated with NIR 20 times over a four-week period and NIR treatment (600-1000 
nm) was associated with a reduction in the size and number of amyloid-β plaques 
in the neocortex and hippocampus. We now report a small pilot double blind, 
placebo-controlled trial (n=11) 6 active, 3 controls and 2 dropouts assessing 
the effect of 28 consecutive, sixminute transcranial sessions of near infrared 
(NIR) stimulation using 1060-1080 nm light emitting diodes. Subjects were 
independently diagnosed with dementia conducted in an outpatient behavioral 
healthcare clinic. IRB approval was obtained through the Quietmind Foundation's 
institutional review Board (IRB). Results showed changes in executive 
functioning; clock drawing, immediate recall, praxis memory, visual attention 
and task switching (Trails A&B) as well as a trend of improved EEG amplitude and 
connectivity measures. Neuroplasticity has also been reported with NIR light 
stimulation and mitochondrial enhancement.