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The Journal of Alzheimer’s Disease is an international multidisciplinary journal to facilitate progress in understanding the etiology, pathogenesis, epidemiology, genetics, behavior, treatment and psychology of Alzheimer’s disease.
The journal publishes research reports, reviews, short communications, book reviews, and letters-to-the-editor. The journal is dedicated to providing an open forum for original research that will expedite our fundamental understanding of Alzheimer’s disease.
Authors: Andorn, Anne C. | Kalaria, Rajesh N.
Article Type: Research Article
Abstract: Oxidative stress may have a key pathogenetic role in neurodegenerative diseases including Alzheimer's disease (AD). While there is evidence that some amyloid-β (Aβ) peptides can initiate oxidative stress at micromolar doses, there is also some evidence that oxidative stress increases the concentration of the β-protein precursor (βPP) and the potential for increased formation of the Aβ peptides. The following studies were performed to test the hypothesis that fragments of βPP could be antioxidants and hence that oxidative stress might be an early event in AD. We found that several fragments of βPP, including the Aβ peptides, inhibit ascorbate-stimulated lipid peroxidation …(ASLP) in membrane fragment preparations of postmortem human brain. In contrast, other fragments of βPP enhance ASLP. These data indicate that βPP or fragments of bPP could play a key role in the redox status of cells and that alterations in bPP processing could have profound effects on the cellular response to oxidative stress. Show more
DOI: 10.3233/JAD-2000-2201
Citation: Journal of Alzheimer's Disease, vol. 2, no. 2, pp. 69-78, 2000
Authors: Pappolla, Miguel A. | Ogden-Epker, Melissa
Article Type: Research Article
DOI: 10.3233/JAD-2000-2202
Citation: Journal of Alzheimer's Disease, vol. 2, no. 2, pp. 79-82, 2000
Authors: Bush, Ashley I. | Atwood, Craig S. | Goldstein, Lee E. | Huang, Xudong | Rogers, Jack
Article Type: Research Article
DOI: 10.3233/JAD-2000-2203
Citation: Journal of Alzheimer's Disease, vol. 2, no. 2, pp. 83-84, 2000
Authors: Summers, William K.
Article Type: Research Article
DOI: 10.3233/JAD-2000-2204
Citation: Journal of Alzheimer's Disease, vol. 2, no. 2, pp. 85-93, 2000
Authors: Samuels, Steven C. | Davis, Kenneth L.
Article Type: Article Commentary
DOI: 10.3233/JAD-2000-2205
Citation: Journal of Alzheimer's Disease, vol. 2, no. 2, pp. 95-96, 2000
Authors: Chen, Ming | Fernandez, Hugo L.
Article Type: Research Article
Abstract: Alzheimer's disease (AD) has been intensively studied for decades, but why has its common pathological cause remained so enigmatic? Our studies have suggested that plaques and tangles occur spontaneously during aging as a result of a natural decline of energy metabolism and Ca2+ signaling, but not necessarily due to conventional pathogens. This view would lead to an unexpected outcome; that is, natural aging plays a more important role in neurodegeneration than is currently recognized. Does this model over-simplify the disease origin? We know that AD-type neurodegeneration typically occurs at the end stages of life when not only do plaques …and tangles appear, but also many other bodily changes as well (bone loss and skin wrinkling, etc). Neurodegeneration differs from the latter changes mainly by “social” consequences, not by “physiological” origin. If neurodegeneration is a natural event, then why do only some people, but not others, develop AD? Obviously, additional factors are required for neurodegeneration to develop into AD. By comparing current models and ruling out other possibilities, we think that several known “risk factors” most likely play a critical role in the late-onset sporadic AD. These risk factors can exert their effects either by providing the conditions for ailing neurons to die (extended longevity and sedentary lifestyle), or by enhancing the individual's “vulnerability” to natural neurodegeneration (low synapse reserve). In this context, late-onset sporadic AD would be similar to many other age-related conditions where perhaps no single pathogen can be held exclusively responsible for most cases; rather, many risk factors are important to allow the initial defect to turn into clinical diseases. Accordingly, these factors should be the primary targets for AD prevention. Yet, some other AD cases, especially the early-onset ones, may be complicated by the concomitant involvement of other diseases in the brain. Show more
Keywords: Alzheimer, aging, calcium, amyloid, presenilin, osteoporosis, atherosclerosis, Parkinson's
DOI: 10.3233/JAD-2000-2206
Citation: Journal of Alzheimer's Disease, vol. 2, no. 2, pp. 97-108, 2000
Authors: Mattson, Mark P.
Article Type: Article Commentary
DOI: 10.3233/JAD-2000-2207
Citation: Journal of Alzheimer's Disease, vol. 2, no. 2, pp. 109-112, 2000
Authors: Price, J.L. | Rubin, E.H. | Morris, J.C.
Article Type: Article Commentary
DOI: 10.3233/JAD-2000-2208
Citation: Journal of Alzheimer's Disease, vol. 2, no. 2, pp. 113-114, 2000
Authors: Khachaturian, Zaven S.
Article Type: Article Commentary
DOI: 10.3233/JAD-2000-2209
Citation: Journal of Alzheimer's Disease, vol. 2, no. 2, pp. 115-116, 2000
Authors: Ghanbari, Hossein A.
Article Type: Article Commentary
DOI: 10.3233/JAD-2000-2210
Citation: Journal of Alzheimer's Disease, vol. 2, no. 2, pp. 117-117, 2000
Authors: Chen, Ming | Fernandez, Hugo L.
Article Type: Article Commentary
DOI: 10.3233/JAD-2000-2211
Citation: Journal of Alzheimer's Disease, vol. 2, no. 2, pp. 119-121, 2000
Authors: Yatin, Servet M. | Varadarajan, Sridhar | Butterfield, D. Allan
Article Type: Research Article
Abstract: Amyloid ß-peptide (Aß) is a 42-43 amino acid peptide known to accumulate in Alzheimer's disease (AD) brain. We previously reported that the neurotoxicity caused by Aß is a result of its associated free radicals, which can play an important role in generating oxidative stress. Aß(25-35)-associated oxidative stress-induced neuronal death in vitro is well established by many laboratories, including ours. However, the oxidative stress-induced by the full-length [Aß(1-42)] peptide is not well investigated. The protective effect of antioxidant vitamin E in full-length peptide-induced oxidative stress also has not been reported. Here, we report that the increased protein oxidation, reactive oxygen species …(ROS) formation, and neurotoxicity induced by Aß(1-42) in primary rat embryonic hippocampal neuronal culture are prevented by the free radical scavenger and antioxidant vitamin E. To test the hypothesis that vitamin E's protective effect may be due to inhibition of fibril formation, electron microscopy studies were undertaken. Vitamin E does not inhibit Aß(1-42) fibril formation, suggesting that the neuroprotection afforded by this molecule stems from other processes, most probably through the scavenging of Aß-associated free radicals. These results may have implications on the treatment of Alzheimer's disease. Show more
Keywords: Aß, amyloid ß-peptide, AD, Alzheimer's disease, APP, amyloid precursor protein, DCF-DA, dicholorofluorescin diacetate, DNPH, 2,4-dinitrophenylhydrazine, PBN, phenyl-a-tertbutyl-nitrone, ROS, reactive oxygen species, SP, senile plaques
DOI: 10.3233/JAD-2000-2212
Citation: Journal of Alzheimer's Disease, vol. 2, no. 2, pp. 123-131, 2000
Authors: Clapp-Lilly, Kimberly L. | Duffy, Lawrence K.
Article Type: Article Commentary
DOI: 10.3233/JAD-2000-2213
Citation: Journal of Alzheimer's Disease, vol. 2, no. 2, pp. 133-135, 2000
Authors: Blanchard, Barbara J. | Hiniker, Anne E. | Lu, Connie C. | Margolin, Yelena | Yu, Amy S. | Ingram, Vernon M.
Article Type: Research Article
Abstract: Aggregation of the Alzheimer amyloid β peptide (Aβ) Ab1-42 forms neurotoxic fibrils. In contact with human neurons the fibrils cause rapid influx of external calcium through AMPA/kainate-channels. If this molecular mechanism reflects in vivo events, it could explain the pathogenesis of Alzheimer's disease; activation of AMPA/kainate channels is therefore a likely target for therapeutic intervention. Here we show that short antagonistic “decoy peptides”, made of D-amino acids, eliminate this “calcium effect” of Ab1-42. Since chronically elevated calcium levels in the disease trigger activation of pathways that lead to neuron dysfunction and cell death, our decoy peptides are obvious candidates …for drug development. Show more
DOI: 10.3233/JAD-2000-2214
Citation: Journal of Alzheimer's Disease, vol. 2, no. 2, pp. 137-149, 2000
Article Type: Abstract
DOI: 10.3233/JAD-2000-2215
Citation: Journal of Alzheimer's Disease, vol. 2, no. 2, pp. 151-191, 2000
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