It starts with misplaced keys and forgotten names. Then it takes conversations, faces, decades of memory. The person is still there, somewhere, losing access to themselves.
Current medications — cholinesterase inhibitors like donepezil and memantine — slow symptom progression modestly but don't alter the disease course. The newer anti-amyloid antibodies (lecanemab, aducanumab) target plaque removal with marginal cognitive benefits and significant side effect risk including brain swelling. No approved drug restores lost function. Standard care focuses on support, safety, and managing behavioral symptoms with antipsychotics. The underlying metabolic failure in brain cells — reduced glucose uptake, mitochondrial dysfunction, vascular insufficiency — remains largely unaddressed.
Shapira et al. (2018) published a landmark study in Aging showing that HBOT at 1.5 ATA improved cerebral blood flow and cognitive performance in elderly patients with significant memory decline. SPECT imaging confirmed increased perfusion in prefrontal and temporal regions — the same areas that deteriorate earliest in Alzheimer's. Patients demonstrated measurable improvements in memory, attention, and information processing speed.1
Hadanny et al. (2020) conducted a prospective trial published in Aging demonstrating that 60 sessions of HBOT improved cognitive function in older adults with objective cognitive decline. The treatment increased cerebral blood flow by an average of 16% in hypoperfused brain regions and was associated with improved amyloid clearance via enhanced glymphatic function.2
Harch et al. (2012) reported in Medical Gas Research a case study of a patient with Alzheimer's-type dementia who received 40 HBOT sessions at 1.5 ATA. PET imaging showed a 38% global increase in brain metabolism, and the patient demonstrated improved cognition, mood, and daily function — improvements that persisted at follow-up.3
Xu et al. (2020) showed in a preclinical study in Neural Regeneration Research that HBOT reduced amyloid-beta plaque deposition, decreased neuroinflammation via microglial modulation, and improved spatial memory in Alzheimer's model animals, clarifying the mechanism by which pressurized oxygen may slow disease progression.4
Saltmarche et al. (2017) published in Photomedicine and Laser Surgery a case series of five patients with mild to moderate dementia treated with transcranial and intranasal PBM at 810nm. After 12 weeks, patients showed significant improvements in MMSE scores, clock drawing, and caregiver-reported function, with reduced anxiety and improved sleep. Effects were sustained with ongoing maintenance treatment.5
Purushothuman et al. (2014) demonstrated in PLOS ONE that near-infrared light at 670nm reduced amyloid-beta plaques and neurofibrillary tangles in Alzheimer's model mice while restoring mitochondrial function in cortical neurons. Treated animals showed significantly improved performance in spatial memory tasks.6
Berman et al. (2017) published a pilot trial in Journal of Alzheimer's Disease using transcranial LED photobiomodulation at 810nm in patients with dementia. After eight weeks of home-based treatment, participants showed significant gains in ADAS-cog scores, improved executive function, and enhanced EEG connectivity patterns consistent with cognitive improvement.7