Presentation Title

The Resistance Against Alzheimer's and its Relationship to Pre-Conditioned Hypoxia

Start Date

November 2016

End Date

November 2016

Location

MSE 103

Type of Presentation

Oral Talk

Abstract

The basic equation was relatively determined: pathology + the brain = Alzheimer’s. Over the years that equation has been greatly extended, but new studies on Asymptomatic Alzheimer’s disease (ASYMAD) urge that it be reconsidered. ASYMAD, a puzzling state characterized by the presence of AD pathology in individuals with normal clinical evaluations, has been previously defined as “pre-clinical” AD. However, as the high frequencies of ASYMAD neuropathology are identified, this state is becoming more appreciated as one of cognitive reserve and pathological resistance. This preliminary study aims to gather the accumulating body of knowledge that reveals the mechanisms involved in the hallmarks of ASYMAD: neuronal hypertrophy and cognitive protection. This study brings additional factor into the unsolved equation, preconditioned hypoxia--a powerful form of cell and cognitive protection. Rationale supporting this new concentration is primarily based on the rising possibility of hypoxic insult as a final ingredient in Alzheimer’s disease, a transitioning factor from a person with MCI to AD. More importantly, the mechanisms and behavior underlying pre-conditioned hypoxia appear to vastly overlap with those underlying the main characteristics of ASYMAD. Together, these observations suggest 1) the natural resistance against Alzheimer’s might be empowered by a natural resistance against hypoxia 2) the resistance against hypoxia constitutes a protective mechanism similar to that of ASYMAD. Systematic methods involved in inducing pre-conditioned hypoxia render its findings much more efficient than that of ASYMAD, which is a phenomenon even less understood than the average symptomatic Alzheimer’s. Therefore, the new approach proposed by this study is to consider pre-conditioned hypoxia as a comparative model in the attempt to understand ASYMAD. It is critical that new efficient methods be considered in light of the fact that ASYMAD’s apparently protective state may shed light on mechanisms blocking the progression of Alzheimer’s disease and permit maintenance of cognitive health.

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Nov 12th, 11:30 AM Nov 12th, 11:45 AM

The Resistance Against Alzheimer's and its Relationship to Pre-Conditioned Hypoxia

MSE 103

The basic equation was relatively determined: pathology + the brain = Alzheimer’s. Over the years that equation has been greatly extended, but new studies on Asymptomatic Alzheimer’s disease (ASYMAD) urge that it be reconsidered. ASYMAD, a puzzling state characterized by the presence of AD pathology in individuals with normal clinical evaluations, has been previously defined as “pre-clinical” AD. However, as the high frequencies of ASYMAD neuropathology are identified, this state is becoming more appreciated as one of cognitive reserve and pathological resistance. This preliminary study aims to gather the accumulating body of knowledge that reveals the mechanisms involved in the hallmarks of ASYMAD: neuronal hypertrophy and cognitive protection. This study brings additional factor into the unsolved equation, preconditioned hypoxia--a powerful form of cell and cognitive protection. Rationale supporting this new concentration is primarily based on the rising possibility of hypoxic insult as a final ingredient in Alzheimer’s disease, a transitioning factor from a person with MCI to AD. More importantly, the mechanisms and behavior underlying pre-conditioned hypoxia appear to vastly overlap with those underlying the main characteristics of ASYMAD. Together, these observations suggest 1) the natural resistance against Alzheimer’s might be empowered by a natural resistance against hypoxia 2) the resistance against hypoxia constitutes a protective mechanism similar to that of ASYMAD. Systematic methods involved in inducing pre-conditioned hypoxia render its findings much more efficient than that of ASYMAD, which is a phenomenon even less understood than the average symptomatic Alzheimer’s. Therefore, the new approach proposed by this study is to consider pre-conditioned hypoxia as a comparative model in the attempt to understand ASYMAD. It is critical that new efficient methods be considered in light of the fact that ASYMAD’s apparently protective state may shed light on mechanisms blocking the progression of Alzheimer’s disease and permit maintenance of cognitive health.