Limits...
Rehabilitating a brain with Alzheimer's: a proposal.

Aranda-Abreu GE, Hernández-Aguilar ME, Manzo Denes J, García Hernández LI, Herrera Rivero M - Clin Interv Aging (2011)

Bottom Line: In spite of the large amount of research going on around the globe and all the information now available about AD, there is still no origin or triggering process known so far.Drugs approved for the treatment of AD include tacrine, donepezil, rivastigmine, galantamine, and memantine.These may delay or slow down the degenerative process for a while, but they can neither stop nor reverse its progression.

View Article: PubMed Central - PubMed

Affiliation: Programa de Neurobiología, Universidad Veracruzana, Xalapa, Mexico. garanda@uv.mx

ABSTRACT
Alzheimer's disease (AD) is the most common neurodegenerative disorder, originating sporadically in the population aged over 65 years, and advanced age is the principal risk factor leading to AD development. In spite of the large amount of research going on around the globe and all the information now available about AD, there is still no origin or triggering process known so far. Drugs approved for the treatment of AD include tacrine, donepezil, rivastigmine, galantamine, and memantine. These may delay or slow down the degenerative process for a while, but they can neither stop nor reverse its progression. Because that this might be due to a lack of effect of these drugs on degenerating neurons, even when they are able to potentiate the brain in nondegenerative conditions, we propose here an alternative therapy consisting of initial repair of neuronal membranes followed by conventional drug therapies. The rehabilitation of neurons in a degeneration process would enable the drugs to act more effectively on them and improve the effects of treatment in AD patients.

Show MeSH

Related in: MedlinePlus

Restoration of the dendritic spine. Dendrites damaged as a result of Alzheimer’s disease would result in abnormal neurotransmission because the receptors are not located in the right site as a result of the effect of neurodegeneration. The repair process is shown, beginning with omega-3 to allow repair of membranes and thus locate the receptors in the right places for effective neurotransmission. Serotonergic neurons would help in the formation of circuits due to the use of serotonin reuptake. Resveratrol and Ginkgo biloba serve as antioxidants and in the process of memory, respectively. Folic acid maintains the integrity of the newly repaired circuits.
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC3066253&req=5

f1-cia-6-053: Restoration of the dendritic spine. Dendrites damaged as a result of Alzheimer’s disease would result in abnormal neurotransmission because the receptors are not located in the right site as a result of the effect of neurodegeneration. The repair process is shown, beginning with omega-3 to allow repair of membranes and thus locate the receptors in the right places for effective neurotransmission. Serotonergic neurons would help in the formation of circuits due to the use of serotonin reuptake. Resveratrol and Ginkgo biloba serve as antioxidants and in the process of memory, respectively. Folic acid maintains the integrity of the newly repaired circuits.

Mentions: Omega-3 acid could help restoration of neuronal membranes to the AD brain, allowing proper positioning of postsynaptic receptors, and enabling existing drug treatment to be more effective. Tau dephosphorylation would restore axonal transport of synaptic vesicles, and thus improve neurotransmitter release at the axon terminals. Once the membranes have been repaired, it would be important to induce the formation and maintenance of new synapses (Figure 1) by fluoxetine or escitalopram and folic acid. Serotonin regulates neuronal morphology and the reconnection between neurons,45 its pathway interacts with that of acetylcholine,46 and it also has a role in memory impairment.47,48 A powerful antioxidant, such as resveratrol, and the activation of memory processes induced by Ginkgo bilboa, would improve the effects of membrane repair and formation of synapses. All of this together might then rehabilitate the AD brain to enable institution of drug treatment producing a better outcome (Figure 2). Ongoing neurodegenerative processes and the mechanisms of action of the drugs available have failed to cure AD,49 because they are brain enhancers.50


Rehabilitating a brain with Alzheimer's: a proposal.

Aranda-Abreu GE, Hernández-Aguilar ME, Manzo Denes J, García Hernández LI, Herrera Rivero M - Clin Interv Aging (2011)

Restoration of the dendritic spine. Dendrites damaged as a result of Alzheimer’s disease would result in abnormal neurotransmission because the receptors are not located in the right site as a result of the effect of neurodegeneration. The repair process is shown, beginning with omega-3 to allow repair of membranes and thus locate the receptors in the right places for effective neurotransmission. Serotonergic neurons would help in the formation of circuits due to the use of serotonin reuptake. Resveratrol and Ginkgo biloba serve as antioxidants and in the process of memory, respectively. Folic acid maintains the integrity of the newly repaired circuits.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3066253&req=5

f1-cia-6-053: Restoration of the dendritic spine. Dendrites damaged as a result of Alzheimer’s disease would result in abnormal neurotransmission because the receptors are not located in the right site as a result of the effect of neurodegeneration. The repair process is shown, beginning with omega-3 to allow repair of membranes and thus locate the receptors in the right places for effective neurotransmission. Serotonergic neurons would help in the formation of circuits due to the use of serotonin reuptake. Resveratrol and Ginkgo biloba serve as antioxidants and in the process of memory, respectively. Folic acid maintains the integrity of the newly repaired circuits.
Mentions: Omega-3 acid could help restoration of neuronal membranes to the AD brain, allowing proper positioning of postsynaptic receptors, and enabling existing drug treatment to be more effective. Tau dephosphorylation would restore axonal transport of synaptic vesicles, and thus improve neurotransmitter release at the axon terminals. Once the membranes have been repaired, it would be important to induce the formation and maintenance of new synapses (Figure 1) by fluoxetine or escitalopram and folic acid. Serotonin regulates neuronal morphology and the reconnection between neurons,45 its pathway interacts with that of acetylcholine,46 and it also has a role in memory impairment.47,48 A powerful antioxidant, such as resveratrol, and the activation of memory processes induced by Ginkgo bilboa, would improve the effects of membrane repair and formation of synapses. All of this together might then rehabilitate the AD brain to enable institution of drug treatment producing a better outcome (Figure 2). Ongoing neurodegenerative processes and the mechanisms of action of the drugs available have failed to cure AD,49 because they are brain enhancers.50

Bottom Line: In spite of the large amount of research going on around the globe and all the information now available about AD, there is still no origin or triggering process known so far.Drugs approved for the treatment of AD include tacrine, donepezil, rivastigmine, galantamine, and memantine.These may delay or slow down the degenerative process for a while, but they can neither stop nor reverse its progression.

View Article: PubMed Central - PubMed

Affiliation: Programa de Neurobiología, Universidad Veracruzana, Xalapa, Mexico. garanda@uv.mx

ABSTRACT
Alzheimer's disease (AD) is the most common neurodegenerative disorder, originating sporadically in the population aged over 65 years, and advanced age is the principal risk factor leading to AD development. In spite of the large amount of research going on around the globe and all the information now available about AD, there is still no origin or triggering process known so far. Drugs approved for the treatment of AD include tacrine, donepezil, rivastigmine, galantamine, and memantine. These may delay or slow down the degenerative process for a while, but they can neither stop nor reverse its progression. Because that this might be due to a lack of effect of these drugs on degenerating neurons, even when they are able to potentiate the brain in nondegenerative conditions, we propose here an alternative therapy consisting of initial repair of neuronal membranes followed by conventional drug therapies. The rehabilitation of neurons in a degeneration process would enable the drugs to act more effectively on them and improve the effects of treatment in AD patients.

Show MeSH
Related in: MedlinePlus