Novel Biomarker (Aβ42) found for Alzheimer's Disease

This report involves the recognition of Aβ42, a protein that function as as a neurotoxin and now attributed to the development of Alzheimer's disease 

Key Takeaways

• Measurement of the rate of cellular amyloid uptake and metabolic production of toxic amyloid species could be used as novel biomarkers for early and/or differential diagnosis of Alzheimer's disease (AD).
  
• Estimated beta-amyloid (Aβ42) cellular uptake can be more than two times greater in AD patients compared to cognitively normal subjects. A less pronounced yet increased uptake rate was also observed in patients with late-onset mild cognitive impairment (MCI).
  
• This increased uptake may prove to be a key mechanism defining age-related AD progression.
  
• ​The increased cellular amyloid uptake in AD and LMCI may lead to quicker disease progression, but early-onset MCI may result from increased production of toxic amyloid metabolites.​

Of particular relevance is that the Aβ42 protein was shown to be significantly reduced in animal trials involving 1072nm photobiomodulation by researchers at Durham University. (Grillo, 2013) showed that this particular protein along with several others were reduce in the animals that showed improved cognitive and behavioral functioning after a trial of light stimulation. This is the same wavelength of light being used in the Neuradiant 1070 4Q transcranial photobiomodulation technology available now through Neuronic Devices Ltd. (neuronic.online) 


(Grillo SL, Duggett NA, Ennaceur A, Chazot PL (2013). Non-invasive infra-red therapy (1072nm) reduces β-amyloid protein levels in the brain of an Alzheimer’s disease mouse model, TASTPM. J Photochem Photobiology B Biology, 123:13–22.)

Full article here: www.medscape.com/viewarticle/