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ISBN:0897667263
Author: John H. Growdon,Switzerland) International Study Group on the Pharmacology of Memory Disorders Associated with Aging. Meeting (6th : 1991 : Zurich
ISBN13: 978-0897667265
Title: Aging and Alzheimer's Disease: Sensory Systems Neuronal Growth, and Neuronal Metabolism (Annals of the New York Academy of Sciences)
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ePUB size: 1806 kb
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Language: English
Category: Medicine and Health Sciences
Publisher: New York Academy of Sciences (December 1, 1991)
Pages: 303

Aging and Alzheimer's Disease: Sensory Systems Neuronal Growth, and Neuronal Metabolism (Annals of the New York Academy of Sciences) by John H. Growdon,Switzerland) International Study Group on the Pharmacology of Memory Disorders Associated with Aging. Meeting (6th : 1991 : Zurich



Bibliography, etc. Note: Includes bibliographical references and index. Personal Name: Growdon, John H. (John Herbert). Meeting (6th : 1991 :, Zurich, Switzerland).

Bondi, M. Houston, W. Eyler, L. & Brown, G. G. (2005). fMRI evidence of compensatory mechanisms in older adults at genetic risk for Alzheimer disease. Neurology, 64, 501–508. PubMedGoogle Scholar. Functional abnormalities of the medial temporal lobe memory system in mild cognitive impairment and Alzheimer’s disease: Insights from functional MRI studies. Neuropsychologia, 46, 1624–1635. Dickerson, B. Sperling, R. Hyman, B. Albert, M. & Blacker, D. (2007b). Clinical prediction of Alzheimer disease dementia across the spectrum of mild cognitive impairment. Archives of General Psychiatry, 64, 1443–1450.

John H. Growdon, MD, is Professor of Neurology at the Harvard Medical School and attending Neurologist at the Massachusetts General Hospital in Boston. Aging and Alzheimer's Disease: Sensory Systems Neuronal Growth, and Neuronal Metabolism. The Molecular Basis Of Dementia.

The current experimental evidences in ALS studies indicate the importance of both response to oxidative stress and inflammatory systems for pathophysiological mechanism of NDs. Interestingly, recent studies have demonstrated that the g chemokine, monocyte chemoattractant protein 1 (MCP-1 or CCL2), is upregulated in the glial cells of spinal cord tissues in SOD1G93A transgenic ALS mice, implicating the role of the brain’s innate immune system and related inflammation in ALS pathophysiology.

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Annals of the New York Academy of Sciences. Detection of entorhinal layer II using 7Tesla magnetic resonance imaging. Augustinack, Jean C; van der Kouwe, Andre J W; Blackwell, Megan L; Salat, David H; Wiggins, Christopher J; Frosch, Matthew P; Wiggins, Graham C; Potthast, Andreas; Wald, Lawrence L and Fischl, Bruce. Age does not increase rate of forgetting over l volumes and visual memory across the adult life-span. Salat, David H; Buckner, Randy L; Snyder, Abraham Z; Greve, Douglas N; Desikan, Rahul S; Busa, Evelina; Morris, John Carl; Dale, Anders M and Fischl, Bruce. segmentation of magnetic resonance images . Fischl, Bruce; Salat, David H; van der Kouwe, Andre J W; Makris, Nikos; Segonne, Florent; Quinn, Brian T and Dale, Anders M.

Neuronal density was quantified using the optical dissector. Results: Our results showed the absence of a significant neuronal loss during aging in non-pathological brains in both sexes. However, we have demonstrated specific punctual significant variations in neuronal density related with the age and gender in some regions of these brains. In fact, we observed a higher neuronal density in CA3 and CA4 hippocampal areas of non-pathological brains of young men compared to women. Objective: The aim of this study is the analysis of neuronal density in four areas of the hippocampus, and entorhinal and frontal cortices to analyze the possible gender influence during normal aging and in Alzheimer's disease (AD). Methods: Human brain tissues of different age and from both sexes, without neurological pathology and with different Braak's stages of AD, were studied.

Annals of the New York Academy of Sciences, 924, 42–52. & McNaughton, N. (1992). Alzheimer's dementia produces a loss of discrimination but no increase in rate of memory decay in delayed matching to sample. Selective attention in a reaching task: Effects of normal aging and Alzheimer's disease. Journal of Experimental Psychology: Human Perception and Performance, 23, 595–608. Leonard, . Crane, . & Milner, B. (1995).

Distinguishing Alzheimer’s disease (AD) from normal aging has been a recurring nosological and diagnostic problem (Drachman, 1983; Berg, 1988; Morris et a. 1991). From a clinical point of view, the idea that mild memory loss is a common concomitant of aging raises a theoretical model whereby AD and aging lie on a continuous spectrum (Bartus et a. 1982; Brayne and Calloway, 1988). Based on the same stereological unbiased methods used in the present study, West et al. (1994) recently reported no change in neuron number in several hippocampal subfields in normal aging, although they did detect neuronal loss in the dentate hilus and subiculum. This pattern of loss contrasted with loss primarily in the CA1 hippocampal region in AD brains.

Working Memory in Aging and Alzheimer's. Bowles, R. and T. A. Salthouse. Assessing the age-related effects of proactive interference on working memory tasks using the Rasch model. Psychology and Aging 18 (2003): 608-615. Lamar, . D. M. Yousem, and S. Resnick. Age differences in orbitofrontal activation: an fMRI investigation of delayed match and nonmatch to sample. Neuroimage 21 (2004): 1368-1376. Aging and emotional memory: The forgettable nature of negative images for older adults. JEP: General 132 (2003): 310-324. Kensinger, E. "Memory for contextual details: Effects of emotion and aging. Psychology and Aging. Trends in Neurosci 27 (2004): 589-594. Toescu, E. Verkhrasky, and P. W. Landfield.

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