Alzheimer''s Disease: What is it After All?

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Preface
Since my publication of Does Alzheimer’s Disease Really Exist? in 2008, several hundred copies of it have been distributed. One translation into Romanian has also been published in Bucharest by a group of geriatrists headed by Dr. Luiza Spiru. She approached me in Athens during the 2nd World Congress on Controversies in Neurology in 2008 through her associate for my permission to translate the book into Rumanian. As she was President of the Rumanian Chapter of The Alzheimer’s Association I agreed and a copy of the book for their translation was provided.
During the Third World Congress on Controversies in Neurology held in Prague, 2009, I was delighted to hear her report in person that the translation had been accomplished; we took a couple of pictures along with three of her associates to celebrate. I wished them luck for the success of the translation, hoping that the Rumanian geriatrists and their patients would be able to make good use of and benefit from my book through their translation.
Positive feedbacks through email correspondences with me and reviews have also appeared since the inception when the book was made available publicly. However, the belief that Alzheimer’s Disease (AD) exists still persists, owing to misjudgments and twistings of historical facts in time and space. For the service to those who have been led to believe that they suffer from AD as well as to the medical community in particular where these patients are likely to be treated as suffering from AD, I have decided to publish this booklet as a sequel. It is intended to counter the common belief that AD exists and challenge for the good of the general public the erroneous diagnosis of dementia as AD often seen in medical practice.
It is rewarding to know, however, that the impact of the first book has alerted the pharmaceutical companies to the extent that even though they invested billions of dollars into the production of various neurotoxic drugs in the past to treat patients with dementia as AD patients, they have now abandoned such productions. I hope that this follow-up booklet will further encourage researchers on dementia to change their courses of research by focusing on dementia, not as a disease, but as a cluster of various forms of the consequences of brain diseases which all result in varying brain atrophies manifesting in behavioral alterations, language disorders among them, which are collectively called dementia.
Each of these brain atrophies may have started lobarly to cause initially what Fischer called in 1907 simple (senile) dementia the form of which may differ, depending on the lesion site at onset; nonetheless, the brain atrophy wherever it may have started in the brain is bound to spread eventually throughout the brain if the patient lives long enough without other complications. During the period of brain atrophy spreading, before the patient dies, he/she is destined to undergo varying stages of deterioration of the brain functions of memory and cognition, ending up eventually in what Fischer called presbyophrenia before death occurs. Presbyophrenia, unlike Kraepelin’s misjudgement, is not an age-dependent simple dementia; rather, it is a devastating total collapse of the brain functions of memory and cognition owing to the evenly atrophic brain caused initially by one or its co-morbidities with other brain diseases.
It is hoped that pharmaceutical companies will take note of the course of deterioration of such brain functions, when targeting the cause of brain atrophy in one form or another resulting in various forms of dementia as the effect. Thus, there is no one-to-one cause-effect relation between brain disease and dementia, because dementia is not one thing but a cluster of behavioral alterations as the effect and more than one brain disease as the cause can lead to brain atrophy to result in dementia. The relations, therefore, have to be many-to-many, occationally one-to-many, in the course of deteriorating behavioral alterations along the time axis, before death occurs. This booklet aims at achieving such an ideal goal as the new perspective of aging resulting in deteriorating behavioral alterations due to wear and tear.

Fred C.C. Peng
Taipei, Taiwan
2012

Table of Contents
Preface v
Acknowledgements    vii
Foreword    ix
1 Early Historical Account
     Abstract   1
     Introduction   1
1. Competition between Arnold Pick and Emil Kraepelin: A Historical View    4
1.1. Pick掇 Line of Thought 6
1.2. Kraepelin掇 Line of Thought    15
2. Conclusion   17
2.1. Dementia Is Not A Disease  18
2.2. Separation of Neurology from Psychiatry May Be A Bliss 19
2 The Core Issues
     Abstract   25
     Introduction   26
1. The Year 1907 Marked The Onset of The Watershed  27
2. Initial Impact of Their Presentations    28
3. Alzheimer Did Not Treat Auguste  30
4. Unfounded Exaggerations after 1907   32
5. Alzheimer’s Manipulation and Kraepelin掇 Power Play 34
6. Fischer’s Contributions 36
7. Fischer’s Contributions in 1907 37
8. Redlich’s Findings in Two Cases 37
9. Fischer’s Disagreement: The Involvement of Glia Cells   38
10. Fischer’s Concept of Miliary Necrosis and Description of Three Stages  41
11. Fischer’s Report of Other Investigators?Research Results   42
12. Fischer’s Implicit Idea of Two Phases of One Pathogenesis  47
     Conclusion 50
3 Is An Animal Model for Human Dementia Plausible?
     Abstract   53
     Introduction   53
     Purpose: To ascertain two things:  55
(1) Are oligomers and amyloid beta proteins the cause of dementia?  55
(2) What Is AD to those ardent supporters of animal models, then?   55
1. Are Oligomers and Amyloid Beta Proteins the Cause of Dementia?   56
1.1. The Notion of A Disease    57
1.2. The Oligomers Are Proteins, Not A Disease  59
2. What Is AD to those Ardent Supporters of Animal Modenls, then?   60
2.1. The Link of Memory Loss/Impairment to A Disease Is Faulty  61
2.2. Oskar Fischer in 1910 already Debated the Issue of Plaques 62
     Conclusion 64
4 Summary and Conclusion
     Summary    68
1. Perusini’s Report on Auguste D. 68
1.1. Perusini’s Casual Observations    68
1.2. Perusini’s Informal (Bedside) Testing 69
1.3. Perusini’s Recording of Her Four Strange Non-language Behaviors   69
1.4. Perusini’s Description of the Autopsied Materials 70
1.5. Perusini’s Report of Her Blindness    71
2. Alzheimer’s Report on Johann F. 71
     Conclusion 73
1. Dementia Is Neither A Disease nor Equivalent to AD   73
2. What Can We Do to Cope with Dementia?    75
3. Possible Solutions   83
Epilogue
     An Open Letter to Science  87
Index   93