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CLINICAL REVIEW:
Alistair Burns and Steve Iliffe
Alzheimer’s disease
BMJ 2009; 338: b158 [Full text]
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Rapid Responses published:

[Read Rapid Response] The patient counts as well
Simon Kenwright   (21 February 2009)
[Read Rapid Response] Biochemical treatment in Alzheimers Disease
Edmond V O`Flaherty   (22 February 2009)
[Read Rapid Response] Alzheimer's Disease Clinical Review: An Error
Sibel Tekin   (2 April 2009)
[Read Rapid Response] Alzheimer’s "disease" is a cerebral amyloidosis
Nikola N. Ilankovic, M.D, Ph.D   (29 September 2009)

The patient counts as well 21 February 2009
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Simon Kenwright,
Retd 2007
East Kent , TN25 6BD

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Re: The patient counts as well

In the recent articles on Alzheimer's disease and the part memory clinics can play in early diagnosis , there has been very little on the impact of the diagnosis on the patient. For many people this will be of greater concern than ,say, a diagnosis of cancer and this impact could well be greater the earlier it is made.It could be seen as doubly threatening as it is likely to have been made at the instigation of a third party and the treatment available very limited. Just as with a cancer diagnosis one would expect the news to be backed by a high degree of accuracy and for those involved to have had adequate training in this aspect of care. If done appropriately ,this may be the optimum time for patients to take part in decisions about their future health care. If done badly the patient may feel that life will no longer be worth living.

Competing interests: Member of Dignity in Dying

Biochemical treatment in Alzheimers Disease 22 February 2009
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Edmond V O`Flaherty,
GP
Gleneagle Greygates Mount Merrion Co Dublin

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Re: Biochemical treatment in Alzheimers Disease

I am a GP but one third of my work is psychiatric and in particular I am interested in getting the biochemistry working normally in addition to using the standard psychiatric treatment. The majority of psychiatric conditions improve with that combination, although OCD responds in only about 15% of cases. I looked at Alzheimers Disease and in particular the biochemical treatment being tried by Pfeiffer Center in Chicago. They believe that the far from perfect performance of the gut at that age is one of the causes and suggest metallothionein promotion to improve the transmission of proteins in the form of amino acids through the gut wall might help. I myself have tried it in only one case -it costs about 50p per day but others thought this was too expensive and would not try it. Happily two years on my patient is doing well and her husband is very happy with the result. I have given details of this and and other aspects of nutrition in mental health at www.omega3.20megsfree.com .The first page will get you on to the Pfeiffer data.

Competing interests: None declared

Alzheimer's Disease Clinical Review: An Error 2 April 2009
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Sibel Tekin,
Global Medical Director
Novartis Pharmaceuticals Corporation East Hanover NJ 07936

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Re: Alzheimer's Disease Clinical Review: An Error

Dear Editor

The recent paper by Burns and Iliffe provided another lucid and comprehensive review about a challenging diease, and it was a pleasure to read. However, I feel I must alert you to a typographical error that might be misleading to some of your readers.

In the section describing pharmacotherapy, "Cholinesterase inhibitors are the mainstay of drug treatment for Alzheimer's disease... all three cholinesterase inhibitors are available in patch form..." In fact, all three cholinesterase inhibitors (rivastigmine, donepezil, galantamine) are available in oral form, and only rivastigmine is available as a patch.

I believe that it is important to point this out because the wrongly suggested parity of administration options is cited to suggest difficulties in choosing between the three drugs. However, for people with Alzheimer's disease or carers wishing to take advantage of the convenience or practical benefits of a modern patch therapy, this might be an important differentiating point.

Small & Dubois (2007) observed that patch therapy might have particular practical advantages for people with Alzheimer's disease, including ease of use and enhanced treatment compliance. Winblad and Machado (2008) suggested that it could allow easier access to higher doses without sacrificing tolerability (this might be an important advantage with these drugs, which show a dose-response relationship).

I hope that the authors will consider these comments in a constructive manner, and I congratulation them once again on their otherwise excellent review.

Sincerely,
Sibel Tekin, MD.

Competing interests: Full time employee of Novartis Pharmaceuticals Corporation

Alzheimer’s "disease" is a cerebral amyloidosis 29 September 2009
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Nikola N. Ilankovic, M.D, Ph.D,
Professor, Head
Belgrade 11000

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Re: Alzheimer’s "disease" is a cerebral amyloidosis

Alzheimer’s "disease" is not one disease with a known cause. It is a histopathological (and clinical) syndrome with many causes.

I think Alzheimer’s "disease" is a CEREBRAL AMYLOIDOSIS, a form and localisation of systemic amyloidosis. Chronic infections and inflammation, most frequently in women, can be a cause of systemic and cerebral amyloidosis, too.

Amyloid A (AA) amyloidosis is the most common form of systemic amyloidosis worldwide. It is characterized by extracellular tissue deposition of fibrils that are composed of fragments of serum amyloid A (SAA) protein, a major acute-phase reactant protein, produced predominantly by hepatocytes. AA amyloidosis occurs in the course of a chronic inflammatory disease of either infectious or noninfectious etiology, TBC, lues, and with certain neoplasms such as Hodgkin disease and renal cell carcinoma.

In developing countries, the most common instigator of AA amyloidosis is chronic infection; in industrialized societies, rheumatic diseases, such as rheumatoid arthritis (RA)- consequence as acute and chronic infections, are the usual stimuli.

In AA amyloidosis, the kidney, liver, spleen and the BRAIN (Ilankovic, 2004) are the major sites of involvement. The tissue fibril consists of a 7500-dalton cleavage product of the SAA protein, an acute- phase protein produced in numerous tissues. The major source of the circulating protein is the hepatocyte. Under the influence of the inflammatory cytokine interleukin (IL)-6, hepatic transcription of the messenger ribonucleic acid (mRNA) for SAA may increase 1000-fold when exposed to an inflammatory stimulus.

Early detection and targeted antiinfective / antiinflammatory therapy of chronic infections and inflammation, can be very effective in reducing many of the consequences: rheumatic disorders, other multisystemic diseases, and systemic (and cerebral) amyloidosis.

Competing interests: None declared