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February 11, 2008

Alzheimers Disease… What’s It Really Like?

By Diane L. Christopher
Buffalo, New York


I would like to dedicate this in Honor of my Beloved Mother, diagnosed with Alzheimers Disease, who passed away last April 22, 2006. Just exactly how many people are familiar with this horrible disease? Some may say they have never heard of it. Others may say it’s “hardening of the arteries.” Some may even say it’s just old age “creeping in.” But, the real truth of the matter is, it’s the most debilitating, demoralizing, destructive, and devastating disease within existence.

Does anyone really know what a person with this disease goes through?

How they spend their hours, their days, their nights, their very existence? Just once, we should try and view the world through their eyes. Just once, we should walk the path they walk. And just once, we should be told we can no longer live on our own. That we are incapable of taking proper care of ourselves.

The trouble is everyone is too busy and too caught up in their own daily lives to feel the pain, the anguish, the fears and tears of a person with this disease . “There but by the Grace of God go I.” Please take a moment to just think about it, as this world they now exist in is very confusing, dark, lonely and at times, almost completely void of reality as we know it. To a person with this disease the world can be a pretty frightening place. A clouded, distorted view of life free of warmth, free of past comforts, and even at times free of love because of lack of understanding.

What have we brought into this world? Nothing! What can we take out of this world when we leave it? Nothing! Just once try to put yourselves in their place. Try once to experience first hand the frustration, the emptiness, and the heartache that that fills their day each and every day.

When was the last time you had to have someone feed you, or the last time you had to have someone dress you, or bathe you? Or comb your hair , or for that matter, brush your teeth? This is merely the beginning as the real heartbreaker is when they can no longer walk or talk, or even swallow their food. Sound horrifying? It is!! Once again, “There but by the Grace of God go I.”

Please try and think long and hard. Please try thinking with your hearts and not your schedules. Please try to take out one hour a week, one hour every two weeks, or possibly just one hour a month. Go and visit a Facility where residents with Alzheimers Disease reside. There is no cost….it’s free. The only thing is it may possibly cost you is a smile, a hug, or a reassuring pat on the shoulder. Perhaps just a listening ear, or a tender loving and caring heart. The rewards reaped will be monumental.

Remember 911? Who could ever forget? But, as the days passed, people seemed to do exactly that. We all returned to our old lives, our old ways of living and our busy schedules. Please don’t let this happen here. The time is here and now. Please give of yourselves, your understanding, your love, your time, and put a smile back upon one face, put back a song within one heart and maybe even wipe away one tear or two from a pair of tired eyes. You will be so very much the richer. But most of all, you will fill someone else’s life with warmth and make a difference in someone’s life that otherwise was quite cold and empty.

May God continue to bless them and you.

Maybe this will help if even in a small way... it is my contribution to all those out there suffering from this disease. And to all the loved ones and friends who are caregivers.

Diane L. Christopher
22 Terry Lane
Buffalo, New York 14225-1340
diane22[at]roadrunner.com

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February 09, 2008

Accidental Memory Stimulation Points at Possible Alzheimer's Treatment

...A study published in the January 29th Annals of Neurology reveals that surgeons operating on an awake obese patient under general anesthesia discovered that brain stimulation evoked detailed autobiographical memories. The procedure was a last attempt to control the patient's morbidly obese weight and involved Bilateral hypothalamic deep brain stimulation. Researchers tried to find appetite-suppressant areas in the hypothalmus.

As surgeons implanted electrodes into the patient's brain, he suddenly began to experience a flood of memories from a visit to a park he had made decades earlier. He recounted events in amazing detail, from the weather to the types of clothes his friends were wearing. As the current on the electrodes intensified, the memories grew richer in detail. He performed better in simple recall tests with the electrodes turned on than when the current was turned off. Subsequently, the same memories were recounted when surgeons at the Toronto Western Hospital applied current to the same area of the brain two months later.

Deep brain stimulation has already shown to be effective against Parkinson's disease. A neurostimulator surgically implanted into the brain of Parkinson's patients results in marked reduction of tremors, rigidity, and stiffness. The patients are also able to increase speed of movement and have less difficulty walking. In the situation of the obese patient, surgeons monitored the changes in brainwave function through EEG monitors and noticed an increase in brainwave frequency. Sufferers of Alzheimer's have decreased brainwave frequency.

Source: associatedcontent.com (9 Feb 2008)

February 01, 2008

Paper Alert by Alzforum: ABCA1 Protects Against Amyloid Deposition

A paper in the January 17 Journal of Clinical Investigation online supports the idea that ABCA1 (ATP-binding cassette A1), a protein transporter involved in lipidation, can protect against amyloid buildup. David Holtzman and colleagues from Washington University, St. Louis, Missouri, overexpressed ABCA1 in PDAPP transgenic mice. First author Suzanne Wahrle and colleagues report that the mice have a very similar phenotype to ApoE-negative animals. Both ABCA1 overexpression and ApoE loss lead to significantly less amyloid-β in the hippocampus than normal PDAPP mice. What little Aβ is present occurs predominantly in the hilus. There is also a dearth of amyloid plaques, as judged by thioflavin S staining. Alzforum first discussed these findings in our report from the Bar Harbor Workshop, Enabling Technologies for Alzheimer Disease Research (see ARF related news story).

ABCA1 seems crucial for loading ApoE with lipid and loss of the transporter leads to reduced levels of ApoE, but not amyloid, in the brain (see ARF related news story). These latest results support the idea that the lipidation status of ApoE is intimately linked with its effect on Aβ processing and aggregation. The data “support the conclusions that increased ABCA1-mediated lipidation of apoE in the CNS can reduce amyloid burden and that increasing ABCA1 function may have a therapeutic effect on AD,” write the authors.—Tom Fagan.

Reference:Wahrle SE, Jiang H, Parsadanian M, Kim J, Li A, Knoten A, Jain S, Hirsch-Reinshagen V, Wellington CL, Bales KR, Paul SM, Holtzman DM. Overexpression of ABCA1 reduces amyloid deposition in the PDAPP mouse model of Alzheimer disease. J. Clin. Invest. 2008 January 17 online. Full Text at J Clin Investigation Abstract

Source: Alzforum research news (22 January 2008) [FullText and comments]

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