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  • JAMA July 25, 2017

    Figure 1: Representative Images of Phosphorylated Tau Pathology at CTE Pathological Stages I and II

    CTE indicates chronic traumatic encephalopathy; NFT, neurofibrillary tangle; ptau, phosphorylated tau. For all images, 10-µm paraffin-embedded tissue sections were immunostained with microscopic mouse monoclonal antibody for phosphorylated tau (AT8) (Pierce Endogen). Positive ptau immunostaining appears dark red, hematoxylin counterstain; calibration bar indicates 100 µm. Stage I CTE is characterized by 1 or 2 isolated perivascular epicenters of ptau NFTs and neurites (ie, CTE lesions) at the depths of the cortical sulci. In stage II, 3 or more cortical CTE lesions are found. All hemispheric tissue section images are 50-µm sections immunostained with mouse monoclonal antibody CP-13, directed against phosphoserine 202 of tau (courtesy of Peter Davies, PhD, Feinstein Institute for Medical Research; 1:200); this is considered to be an early site of tau phosphorylation in NFT formation. Positive ptau immunostaining appears dark brown. A, Former college football player with stage I CTE. Two perivascular ptau CTE lesions are evident at sulcal depths of the frontal cortex; there is no neurofibrillary degeneration in the medial temporal lobe (open arrowhead). Perivascular CTE lesion: neurofibrillary tangles and dot-like and threadlike neurites encircle a small blood vessel. B, Former NFL player with stage II CTE. There are multiple perivascular ptau CTE lesions at depths of sulci of the frontal cortex; there is no neurofibrillary degeneration in the medial temporal lobe (open arrowhead). Perivascular CTE lesion: a cluster of NFTs and large dot-like and threadlike neurites surround a small blood vessel.
  • JAMA July 25, 2017

    Figure 2: Representative Images of Phosphorylated Tau Pathology at CTE Pathological Stages III and IV

    CTE indicates chronic traumatic encephalopathy; NFT, neurofibrillary tangle; ptau, phosphorylated tau. For all images, 10-µm paraffin-embedded tissue sections were immunostained with microscopic mouse monoclonal antibody for phosphorylated tau (AT8) (Pierce Endogen). Positive ptau immunostaining appears dark red, hematoxylin counterstain; calibration bar indicates 100 µm. In stage III CTE, multiple CTE lesions and diffuse neurofibrillary degeneration of the medial temporal lobe are found. In stage IV CTE, CTE lesions and NFTs are widely distributed throughout the cerebral cortex, diencephalon, and brain stem. All hemispheric tissue section images are 50-µm sections immunostained with mouse monoclonal antibody CP-13, directed against phosphoserine 202 of tau (courtesy of Peter Davies, PhD, Feinstein Institute for Medical Research; 1:200); this is considered to be an early site of tau phosphorylation in NFT formation. Positive ptau immunostaining appears dark brown. A, Former NFL player with stage III CTE. There are multiple large CTE lesions in the frontal cortex and insula; there is diffuse neurofibrillary degeneration of hippocampus and entorhinal cortex (black arrowhead). Perivascular CTE lesion: a dense collection of NFTs and large dot-like and threadlike neurites enclose several small blood vessels. B, Former NFL player with stage IV CTE. There are large, confluent CTE lesions in the frontal, temporal, and insular cortices and there is diffuse neurofibrillary degeneration of the amygdala and entorhinal cortex (black arrowhead). Perivascular CTE lesion: a large accumulation of NFTs, many of them ghost tangles, encompass several small blood vessels.
  • JAMA March 5, 2008

    Figure: Neuronal Map

    A mouse neuron reveals multiple neurites budding from the neuronal body. Researchers have constructed a map of neuronal proteins to study neurite development and function.
  • Neuronal Map

    Abstract Full Text
    JAMA. 2008; 299(9):1008-1008. doi: 10.1001/jama.299.9.1008-b
  • JAMA March 22, 2000

    Figure 2: Tau Neuropathology in the Frontal Cortex

    Tau neuropathology was evaluated using the conformation-dependent monoclonal antibody MC1 (counterstained with toluidine blue O, original magnification ×250). The staining pattern was used to classify the subjects into 1 of 3 categories (see also Table 5). A, No MC1 staining. B, MC1 staining of neurites only (arrows). C, MC1 staining of neurites, neuritic plaques, and neurofibrillary tangles. AD indicates Alzheimer disease.
  • JAMA May 8, 2002

    Figure 1: Morphology and Distribution of Neuritic Plaques and Neurofibrillary Tangles

    A, Neuritic plaque (labeled with a monoclonal antibody for human amyloid peptide using diaminobenzidine combined with hematoxylin counterstain, × 2500 magnification). B, Distribution of neuritic plaques in the cerebral cortex. C, Neurofibrillary tangle (Gallyas silver stain; × 2500 magnification). D, Distribution of neurofibrillary tangles in the cerebral cortex.
  • Clinical Reactions Following Rubella Vaccination: A Prospective Analysis of Joint, Muscular, and Neuritic Symptoms

    Abstract Full Text
    JAMA. 1972; 220(12):1569-1572. doi: 10.1001/jama.1972.03200120021004
  • Association of Seafood Consumption, Brain Mercury Level, and APOE ε4 Status With Brain Neuropathology in Older Adults

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    JAMA. 2016; 315(5):489-497. doi: 10.1001/jama.2015.19451

    This cohort study describes correlations and associations between premortem seafood intake, postmortem brain mercury levels, and postmortem Alzheimer disease neuropathology in older adults.

  • Use of Florbetapir-PET for Imaging β-Amyloid Pathology

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    JAMA. 2011; 305(3):275-283. doi: 10.1001/jama.2010.2008
  • Clinicopathological Evaluation of Chronic Traumatic Encephalopathy in Players of American Football

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    JAMA. 2017; 318(4):360-370. doi: 10.1001/jama.2017.8334

    This case series investigated the neuropathological and clinical features of deceased football players with chronic traumatic encephalopathy whose brains were donated for research.

  • Prevalence of Amyloid PET Positivity in Dementia Syndromes: A Meta-analysis

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    JAMA. 2015; 313(19):1939-1950. doi: 10.1001/jama.2015.4669

    This participant-level meta-analysis estimates the prevalence of PET scan–measured amyloid in Alzheimer disease participants and its associations with age, sex, education, cognitive function, and APOE genotype.

  • Prevalence of Cerebral Amyloid Pathology in Persons Without Dementia: A Meta-analysis

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    JAMA. 2015; 313(19):1924-1938. doi: 10.1001/jama.2015.4668

    This meta-analysis explores the association of amyloid pathology with age, APOE genotype, sex, education, and presence of cognitive impairment among persons without dementia.

  • Correlation Between Elevated Levels of Amyloid β-Peptide in the Brain and Cognitive Decline

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    JAMA. 2000; 283(12):1571-1577. doi: 10.1001/jama.283.12.1571
  • Association of an Inherited Genetic Variant With Vincristine-Related Peripheral Neuropathy in Children With Acute Lymphoblastic Leukemia

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    JAMA. 2015; 313(8):815-823. doi: 10.1001/jama.2015.0894

    This genome-wide association study performed among children with acute lymphoblastic leukemia (ALL) found that an inherited polymorphism in the promoter region of CEP72 was associated with increased risk and severity of vincristine-related peripheral neuropathy.

  • Cholinergic Markers in Elderly Patients With Early Signs of Alzheimer Disease

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    JAMA. 1999; 281(15):1401-1406. doi: 10.1001/jama.281.15.1401
  • Brain Infarction and the Clinical Expression of Alzheimer Disease-Reply

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    JAMA. 1997; 278(2):114-114. doi: 10.1001/jama.1997.03550020046024
  • Predicting Progression of Alzheimer Disease

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    JAMA. 1997; 277(24):1933-1934. doi: 10.1001/jama.1997.03540480033030
  • Predicting Progression of Alzheimer Disease-Reply

    Abstract Full Text
    JAMA. 1997; 277(24):1934-1934. doi: 10.1001/jama.1997.03540480034031
  • Biochemical Assay of Alzheimer's Disease—Associated Protein(s) in Human Brain Tissue: A Clinical Study

    Abstract Full Text
    JAMA. 1990; 263(21):2907-2910. doi: 10.1001/jama.1990.03440210057032