Dementia and Alzheimer Rehabilitation

Biography

Biography: Robert Joseph Hedaya

Abstract

It is widely recognized that the current treatment approach to subjective and mild cognitive impairment (SCI, MCI) and early dementia offers little in the way of efficacious treatment. Decades of research based on various linear models (e.g., amyloid, acetylcholine) with targeted pharmaceutical treatments have failed to produce clinically meaningful results. On the other hand, basic science and systems biology have identified and elucidated multiple modifiable (and mutually interacting) pathophysiological systems which increase vulnerability to neurodegenerative disorders such as SCI, MCI and various dementias. The majority cases of dementia are not unitary in etiology, but rather involve disturbances of multiple systems and are thus pathophysiologically impure. Even such APOE4 homozygotes generally have multiple contributing pathophysiologies, the etiological imprecision of our diagnostic terminology and continued use of a linear medical paradigm results in dismissal of relevant and modifiable pathophysiological contributors to dementia. Hence, diagnostic imprecision must be replaced with etiological precision. Underlying pathophysiological processes which are involved in cognitive decline include: central insulin resistance, mitochondrial and oxidative dysfunction, loss of trophic (nutrient, hormonal, immune, enrichment) support, immune dysfunction and infection, toxicity, cardio-vascular dysfunction, trauma, structure and lifestyle. The clear association between these pathophysiologies, their clinically measurable biometric parameters, and cognitive decline provides a clear treatment map, which is being used to reverse SCI, MCI and early to mid-stage dementia. A large trial of the functional medicine method is currently funded. This presentation will review the evidence and a series of cases demonstrating stabilization and recovery of cognitive function in these disorders.