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Int J Physiol Pathophysiol Pharmacol 2011;3(2):133-139.
Review Article
Bioenergetics breakdown in Alzheimer’s disease: targets for new therapies
Uday Saxena
R and D Strategy, Kareus Therapeutics, SA, Switzerland
Received May 31, 2011; accepted June 8, 2011; Epub June 12, 2010; Published June 30, 2011
Abstract: Alzheimer’s disease is rapidly growing worldwide and yet there is no cure for it. Currently available drugs only provide
symptomatic relief and do not intervene in disease process sufficiently enough to prevent or cure it. Characteristic features of this
disease are decline in neuronal mass and cognitive functions. The most dominant hypothesis proposed for pathogenesis of this
disease is called “amyloid hypothesis”. It states that excessive production of amyloid peptides called abeta peptides (Ab) is the
underlying cause of neuronal death and dysfunction. However, recent drugs designed based on amyloid hypothesis have failed in
clinical trails, demanding fresh assessment. Early and persistent molecular events in this disease progression are energy deficiency
and high oxidative stress in the neurons. Our review will put together a disease model based on known human and animal data with
regards to breakdown in neuronal energy generation. The model will integrate energy deficits as the cause of neuronal dysfunction and
abeta peptide production culminating in catastrophic loss of cognitive functions. Finally, based on this model, we will also suggest
enzyme targets in neuronal bioenergetics pathway for design and development of new disease modifying therapies.
(IJPPP1105004).
Keywords: Alzheimer’s disease, amyloid hypothesis, neuronal energy, new therapeutics
Full Text PDF
Address all correspondence to:
Uday Saxena, PhD
40 rue Fritz-Courvoiser
2300 La Chaux-de-Fonds
Switzerland.
E-mail: usaxena@kareustherapeutics.com
Review Article
Bioenergetics breakdown in Alzheimer’s disease: targets for new therapies
Uday Saxena
R and D Strategy, Kareus Therapeutics, SA, Switzerland
Received May 31, 2011; accepted June 8, 2011; Epub June 12, 2010; Published June 30, 2011
Abstract: Alzheimer’s disease is rapidly growing worldwide and yet there is no cure for it. Currently available drugs only provide
symptomatic relief and do not intervene in disease process sufficiently enough to prevent or cure it. Characteristic features of this
disease are decline in neuronal mass and cognitive functions. The most dominant hypothesis proposed for pathogenesis of this
disease is called “amyloid hypothesis”. It states that excessive production of amyloid peptides called abeta peptides (Ab) is the
underlying cause of neuronal death and dysfunction. However, recent drugs designed based on amyloid hypothesis have failed in
clinical trails, demanding fresh assessment. Early and persistent molecular events in this disease progression are energy deficiency
and high oxidative stress in the neurons. Our review will put together a disease model based on known human and animal data with
regards to breakdown in neuronal energy generation. The model will integrate energy deficits as the cause of neuronal dysfunction and
abeta peptide production culminating in catastrophic loss of cognitive functions. Finally, based on this model, we will also suggest
enzyme targets in neuronal bioenergetics pathway for design and development of new disease modifying therapies.
(IJPPP1105004).
Keywords: Alzheimer’s disease, amyloid hypothesis, neuronal energy, new therapeutics
Full Text PDF
Address all correspondence to:
Uday Saxena, PhD
40 rue Fritz-Courvoiser
2300 La Chaux-de-Fonds
Switzerland.
E-mail: usaxena@kareustherapeutics.com
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