No, cell death is not relevant at all. Alzheimer's is initiated by the precipitation of aluminosilicates in the brain. All that follows: amyloid deposition, tau generation, cell death, tangles, dementia, calcium deposits, whatever, are consequences of the initiating event. Unfortunately, the Good Ole Boys of Alzheimer's research are not giving the rest of you permission to think that way right now. Peer pressure has all of you programmed to focus upon biochemical mumbo-jumbo and you will continue doing exactly that.

View all comments by Colin Meyer

Obviousell death is the target. That is why I choose research into what causes the cell death. Eradicating the cause will eradicate the cell death. Is this not the "chicken or egg question"? To raise the dead is not the cure, the cure is to stop the death in the first place.

View all comments by jan keegan ronk

The main target should be cell-specific carbonic anhydrase enzymes. This target almost explains the pathophysiology of aging and disorders of aging in humans.

Determining which one or more cell-specific carbonic enzymes is present in decreased amounts and then administering one or more compounds that increase the level of one or more cell-specific carbonic enzymes.

The progressive decline of cell-specific carbonic anhydrase enzymes due to normal aging plus diseases or conditions that further reduce the levels of cell-specific carbonic anhydrase enzymes accelerates cellular death such as found in Alzheimer's disease.

Alzheimer's disease is an accelerated disease of aging. It is accelerated due to conditions or diseases that further reduce cell-specific carbonic anhydrase enzymes. These diseases or conditions could be: defective gene-linked carbonic anhydrase enzymes, neurotoxic elements such as aluminum, lead, mercury, iron, copper, infections or infestations, traumas, strokes, amyloid deposits, cholesterol deposits or other conditions or diseases that alter the...  Read more

The main target should be cell-specific carbonic anhydrase enzymes. This target almost explains the pathophysiology of aging and disorders of aging in humans.

Determining which one or more cell-specific carbonic enzymes is present in decreased amounts and then administering one or more compounds that increase the level of one or more cell-specific carbonic enzymes.

The progressive decline of cell-specific carbonic anhydrase enzymes due to normal aging plus diseases or conditions that further reduce the levels of cell-specific carbonic anhydrase enzymes accelerates cellular death such as found in Alzheimer's disease.

Alzheimer's disease is an accelerated disease of aging. It is accelerated due to conditions or diseases that further reduce cell-specific carbonic anhydrase enzymes. These diseases or conditions could be: defective gene-linked carbonic anhydrase enzymes, neurotoxic elements such as aluminum, lead, mercury, iron, copper, infections or infestations, traumas, strokes, amyloid deposits, cholesterol deposits or other conditions or diseases that alter the blood-brain barrier and displace the zinc in the cell-specific carbonic anhydrase enzymes.

Glial cells in the synapse such as astrocytes modulate the transmission of information between neurons; cell death in this region causes synaptic dysfunction. Astrocytes are supposed to have originated from carbonic anhydrase enzymes. Astrocytes are the most abundant glial cell types in the brain. They provide metabolic and trophic support to neurons and modulate synaptic activity.

Neurons and other supporting cells in the brain are fueled by H+(ATP) for them to function and are produced by cell-specific carbonic anhydrase enzymes.

CA I, II, III are cytosolic
CA IV and VII are membrane-bound
CA V is mitochondrial
CA VI is secretory—taste and smell

References:
Takuma K. Baba A, Matsuda T. Astrocyte apoptosis: implications for neuroprotection. Prog Neurobiol. 2004 Feb;72(2):111-27. Review. Abstract

Reddy LV et al. Glial cells maintain synaptic structure and function and promote development of the neuromuscular junction in vivo. Neuron. 2003 Oct 30;40(3):563-80. Abstract

Cammer W, Chang H. Carbonic anhydrase in distinct precursors of astrocytes and oligodendrocytes in the forebrains of neonatal and young rats. Brain Res Dev Brain Res. 1992 Jun 19;67(2):257-63. Abstract

FASB J 2003 Mar 17(3): 341-8 Hanson et al--glial cells interact extensively with neuronal elements in the brain influencing their activity.

WIPO (World Intellectual Property) WO-03070167A3 "Therapeutic and Prophylactic Treatment of Aging and Disorders of Aging in Humans. Victorio C. Rodriguez

View all comments by Victorio Rodriguez

Would love to participate in research. My mother was diagnosed some 6 years ago and is in latter states, bedfast. I am a RN and have worked in MH most of my nursing career. I am POA for my mother. I am 52 years old, single and will devote, in some way , efforts to treat and prevent this horrible disease. THANKS! for all you do! Kathy

View all comments by kathy benz

I would like to see research done on the effects cholesterol lowering drugs have on patients with dementia and alzheimers. I believe these drugs have a direct effect on the brain and contribute to dementia and Alzheimer's. I also believe after taking these drugs for a long period the damage they cause on the brain is not reversible.

View all comments by marva evans