Abstract

Despite the current belief that there is no effective treatment for Alzheimer’s Disease (AD), one emerging modality may change this belief: Photobiomodulation (PBM). It has credible mechanisms and growing evidence to support its case. Transcranial PBM for AD is a single intervention with multiple pathway mechanisms stemming from delivering low energy near infrared (NIR) light to the mitochondria in brain cells. The mechanisms involve the activation of gene transcription that lead to neuronal recovery, removal of toxic plaques, normalizing network oscillations that can lead to improved cognition and functionality. When PBM is delivered at 810 nm wavelength and pulsed at 40 Hz, early evidence suggests that very significant outcomes are possible. Literature related to PBM and AD has covered in vitro cellular, animal and human case reports, with promising results. They warrant robust randomized trials which are either ongoing or ready to start. The evidence in human studies is manifested in assessment scales such ADAS-cog, MMSE, and ADAS-ADL, and are supported by fMRI imaging and EEG.

Highlights

  • It is widely accepted that there is no effective treatment for Alzheimer’s disease (AD)

  • The mechanisms involve the activation of gene transcription that lead to neuronal recovery, removal of toxic plaques, normalizing network oscillations that can lead to improved cognition and functionality

  • It has been demonstrated that mitochondrial dysfunction can push amyloid precursor protein (APP) processing towards the formation of Aβ production [17] [18] [19], suggesting that mitochondrial dysfunction is a factor driving the amyloid cascade resulting in further damage to mitochondria, leading to a self-feeding feedback loop

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Summary

Introduction

It is widely accepted that there is no effective treatment for Alzheimer’s disease (AD). It is widely accepted that no single drug can be the solution—requiring a cocktail combination, and largely hypothesizing that the disease should be addressed at the pre-symptomatic or prodromal stages [2]. The fundamental mechanism is understood to be in the modulation of mitochondrial activity, which will be the hypothetical basis for the effectiveness of PBM to address AD. This manuscript will be a discussion about how PBM has the bases to improve AD conditions and the accumulated related evidence to support this proposition at the time of writing

Pathophysiology to Target
The Futility of Single-Protein Targeting
Going More Basic to Target the Mitochondria
Photobiomodulation Modulates Mitochondrial Function
The Progress of Clinical Evidence with Photobiomodulation
Evidence with Animal Models
Human Clinical Studies with Photobiomodulation on Dementia
Parameters and Their Rationale
The Default Mode Network
Gamma Pulse Frequency at 40 Hz
Findings
The Future of Photobiomodulation as a Treatment for Alzheimer’s Disease
Full Text
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