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FIGURE 8–7. Histopathology images: -amyloid plaques, neuritic plaques, and neurofibrillary tangles in Alzheimer's disease.A, Four recognized stages of neuritic plaque development revealed by the Bielschowsky silver technique. Top left: Diffuse plaque composed mostly of -amyloid (A) peptide without increased density of neurites. Top right: Primitive plaque consisting of A peptide accumulation and increased numbers of nonenlarged neurites. Bottom left: Mature plaque with a densely stained central A amyloid core surrounded by greatly enlarged dystrophic neurites. Bottom right: Burned-out (end-stage) plaque consisting of an isolated mass of A amyloid. B, The classic mature neuritic plaque, about 100 m in diameter, containing a pale staining amyloid core at its center that is surrounded by a halo of dystrophic (enlarged) neurites. Bielschowsky silver technique. C, A mature neuritic plaque with enlarged dystrophic neurites but no amyloid core. D, High magnification view of neurofibrillary tangles, which appear coarse and stain darkly by the Bielschowsky silver technique.Source. Reprinted from Davis RL, Robertson DM (eds): Textbook of Neuropathology, 3rd Edition, Baltimore, MD, Williams & Wilkins, 1997. Copyright 1997, Williams & Wilkins. Used with permission.

FIGURE 8–8. Schematic view of the main pathological events in Alzheimer's disease.Amyloid precursor protein (APP) (1) is released into the media after cleavage by -secretase to form the soluble APP (2). Conversely, APP may be internalized (3) and cleaved by - and -secretases to form -amyloid (A) fragments (4). The protein A aggregates (5) in fibrillar nonsoluble material to compose the core of the neuritic plaque (6). Neurofibrillary tangles form (7). The neurotoxicity of tau and amyloid results in oxidative stress, with increased intracellular reactive oxygen species (ROS), and disruption of structures involved in ion homeostasis such as ion-motive adenosine triphosphatases (8). Inflammatory responses with reactive glial cells (9) lead to production of cytokines and complement. Possibly playing key roles are membrane receptors such as class A scavenger receptor or receptor for advanced glycation end products (10). Global decrease occurs in neurotransmitters, including acetylcholine (11).Potential pharmacological targets: -amyloid protein metabolism (1–5) and aggregation (6); tau protein metabolism (7); oxidative stress, acting via calcium channels (8); inflammatory response (9, 10); neurotransmitter modulation (11); and neuroprotection.Source. Reprinted with permission from Felician O, Sandson TA: "The Neurobiology and Pharmacotherapy of Alzheimer's Disease." Journal of Neuropsychiatry and Clinical Neuroscience 11:19–31, 1999. Copyright 1999, American Psychiatric Press, Inc.

FIGURE 8–9. T2 magnetic resonance image of vascular dementia, multi-infarct type, in a patient with diabetes mellitus and hypertension.The bilateral, symmetrical pattern of white matter lesions is characteristic of small-vessel arterial disease. Enlarged sulci are consistent with associated parenchymal loss.Source. Reprinted with permission from Yock DH: Imaging of CNS Disease: A CT and MRI Teaching File. St. Louis, MO, Mosby–Year Book, Inc., 1991.

FIGURE 8–10. Histopathology images: Lewy body variant of Alzheimer's disease.In this patient with dementia, the number of plaques and tangles in the neocortex was borderline for the diagnosis of Alzheimer's disease. A, The substantia nigra showed a moderate degree of nerve cell loss and small numbers of Lewy bodies. B, Ubiquitin immunohistochemistry revealed multiple Lewy bodies in nerve cells of the cingulate gyrus.Source. Reprinted from Davis RL, Robertson DM (eds): Textbook of Neuropathology, 3rd Edition. Baltimore, MD, Williams & Wilkins, 1997. Copyright 1997, Williams & Wilkins. Used with permission.

FIGURE 8–11. Magnetic resonance image of hippocampal volume (arrows) in a healthy control subject (A) and a patient with Alzheimer's disease and hippocampal atrophy (B).Source. Reprinted with permission from Foster NL, Minoshima S, Kuhl DE: "Brain Imaging in Alzheimer Disease," in Alzheimer Disease, 2nd Edition. Edited by Terry RD, Katzman R, Bick KL, et al. Philadelphia, PA, Lippincott Williams & Wilkins, 1999, p. 69, Figures 2A and 2B. Copyright 1999, Lippincott Williams & Wilkins.

FIGURE 8–12. Fluorodeoxyglucose positron emission tomography study of a healthy older control subject and a patient with Alzheimer's disease (AD).The patient demonstrates bilateral temporal and parietal hypometabolism with some involvement of the posterior cingulate gyrus and relative preservation of primary cortex and basal ganglia. Metabolic activity is greatest in the visual cortex.Source. Reprinted with permission from Valk PE, Bailey DL, Townsend DW, et al.: Positron Emission Tomography: Basic Science and Clinical Practice. London, Springer-Verlag, 2003, pp. 343, 344.

FIGURE 8–13. Fluorodeoxyglucose positron emission tomography study of a patient with late-stage Alzheimer's disease.This patient shows widespread hypometabolism that is still most pronounced in temporal and parietal cortex and maximal in the left hemisphere (right side of the image). There is relative preservation of metabolism in visual cortex and sensorimotor cortex bilaterally.Source. Reprinted with permission from Valk PE, Bailey DL, Townsend DW, et al.: Positron Emission Tomography: Basic Science and Clinical Practice. London, Springer-Verlag, 2003, pp. 343, 344.
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TABLE 8–9. Diagnostic features of the dementias
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TABLE 8–10. Cortical and subcortical dementia types
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TABLE 8–11. Established and proposed risk factors for dementia of the Alzheimer's type
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TABLE 8–12. Potentially reversible etiologies of dementia
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TABLE 8–13. Psychiatric differential diagnosis of dementia
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TABLE 8–14. Laboratory tests for dementia workup
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TABLE 8–15. Dementia pharmacotherapy

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