The 32nd SBCN Annual Meeting took place on Wednesday, April 20, 2016 during the annual AAN meeting. The updated format for the 2016 meeting was well received. It offered an opportunity to connect informally with friends and colleagues in the field at the AAN Meeting. Participants learned about colleagues’ latest research initiatives, and were able to speak directly with the 2016 Geschwind Prize Winner and the 2016 SBCN Lifetime Achievement Award Winner.
Albert M. Galaburda, M.D. was the 2016 Lifetime Achievement Award winner. Dr. Galaburda is the Emily Fisher-Landau Professor of Neurology and Neuroscience at Harvard Medical School. He also co-directs the Mind Brain Behavior Interfaculty Initiative at Harvard University and is an attending neurologist at Beth Israel Deaconess Medical Center. He trained in neurology under Norman Geschwind at what is now Boston Medical Center. His clinical and research expertise is in the field of cognitive neurology with a special focus on learning and attention disorders as they affect adults.
The 2016 Norman Geschwind Prize Winner was Madhav Thambisetty, M.D., Ph.D. is a Clinical Investigator and Chief of the Unit of Clinical and Translational Neuroscience at the National Institute on Aging/Intramural Research Program. His research focuses on enhancing the understanding of disease mechanisms operating in Alzheimer’s Disease and identifying novel biomarkers that might predict disease before the onset of clinical symptoms. He also evaluates and cares for patients with memory disorders at the Johns Hopkins Bayview Memory and Alzheimer’s Treatment Center.
At the 2015 Annual Meeting of the American Academy of Neurology, Kenneth Heilman from the University of Florida and Nicholas Milano from the Medical University of South Carolina presented “Highlights in Behavioral Neurology.” The objective of this session was to highlight and foster discussion of some of the most interesting and important research presented at the AAN meeting. The following is a summary of the abstracts presented.
Cerebral amyloidosis is associated with white matter hyperintensity independent of vascular risk factor history
Julia A. Scott, Duygu Tosun-Turgut, Meredith Braskie, Paul Thompson, Michael Weiner, Charles DeCarli, Owen T. Carmichael
This study aimed to assess the association between cerebral amyloid burden and white matter hyperintensities (WMH) on magnetic resonance images in individuals with varying vascular risk profiles. Using participants from the Alzheimer’s disease Neuroimaging Initiative-2, this study compared WMH volumes with amyloid burden (measured with CSF and PET imaging) and vascular history. The authors found that greater amyloid burden and hypertension history were independently associated with greater WMH volume. Greater amyloid burden was even associated with WMH in individuals with no history of hypertension and normal current blood pressure. WMH are commonly found in patients with Alzheimer’s disease and have been thought of as a marker of cerebral small vessel disease. This study shows that amyloid may be contributing to the generation of WMH and should be considered in their interpretation.
Neural correlates of action recognition and object knowledge in neurodegenerative disease
Miguel A. Santos, Ignacio Illan-Gala, Giulia Vinceti, Maria Luisa Mandelli, Honey Hubbard, Zachary A. Miller, Gil D. Rabinovici, Bruce L. Miller, Maria Luisa Gorno-Tempini
This study aimed to identify the neuroanatomical correlates of action recognition and its relation to object knowledge. Groups consisted of subjects with 1) Alzheimer’s disease (AD) spectrum neurodegenerative disease (early onset AD, logopenic variant primary progressive aphasia (PPA), posterior cortical atrophy), 2) Non-AD spectrum neurodegenerative disease (nonfluent variant PPA, corticobasal degeneration, progressive supranuclear palsy, behavioral variant frontotemporal dementia), 3) semantic variant PPA, and 4) healthy controls. Subjects completed 3 tasks: an action recognition task where they had to match a video of a pantomime (i.e., a hand using an imaginary key) with the correct object (answer: key), a word-picture matching task, and a hand matching task (match hands in different orientations). All subjects also received a 3T structural MRI of their brain, and a whole brain voxel-wise multiple linear regression analysis was performed to identify voxels highly correlated with performance on the action recognition task. The authors found that all groups were significantly worse than controls on the action recognition task and that it correlated with voxels in the bilateral frontal and left posterior temporal and inferior parietal lobes. When controlling for the word picture and hand matching tasks, only the AD spectrum group remained significantly different from controls on the action recognition task, and the task correlated with voxels in the left mid-posterior temporal and inferior parietal lobes. The authors concluded that left mid-posterior temporal and inferior parietal areas are critical for deriving meaning from dynamic gestures, and that AD spectrum disorders show particular impairment in this aspect of action recognition.
Validation of olfactory deficit as a biomarker of AD
Chaitanya V. Amrutkar, Matthew R. Woodward, Harshit C. Shah, Ralph Benedict, Sanjanaa Rajakrishnan, Rachelle S. Doody, Li Yan, Kinga Szigeti
An odor identification deficit (OID) has been associated with both AD and amnestic mild cognitive impairment (aMCI). This study aimed to determine a battery of smell identification tests which maximized sensitivity and specificity to detect early AD and aMCI. All subjects received the full University of Pennsylvania Smell Identification Test (UPSIT). The ROC area under the curve (AUC) for identifying an amnestic disorder (AD or aMCI), and AD alone, was similar for the 40 item UPSIT, the top 10 smells in this study, and the 10 item subset previously proposed by Tabert. This is important as the 10-item subtest decreases the time to administer the test by 75% to 5 minutes. Non-smeller status based on a cutoff of 7 (7 or less= nonsmeller) had a sensitivity of 74% and a specificity of 71% for identifying an amnestic disorder (AD or aMCI). In the longitudinal component of this study, 36.4% of non-smeller patients with aMCI converted to AD, while only 17.3% of patients with intact olfaction converted to AD. The ROC AUC for conversion to AD was 0.62, which is comparable to CSF biomarkers (0.63-0.67) and somewhat inferior to structural MRI (0.69-0.73). This study emphasizes that a short 10-item assessment of an OID is a potential cheap, noninvasive, and accurate biomarker for AD.
In the discussion of this paper it was noted how important it may be to have a simple test that could: 1) help to confirm the diagnosis of early AD and 2) could be given to patients with MCI to learn which patients would be most likely to develop AD.
Psychological Stress and Age-Related Memory decline
Richard J. Caselli, Amylou C. Dueck, Dona Locke, Bryan K. Woodruff, Charlene Hoffman-Snyder, Yonas Geda
Chronic stress has been associated with a variety of functional and structural changes in the prefrontal and hippocampal areas of the brain, and has also been associated with dementia. This study aimed to assess the affect of stress vulnerability on age-related memory decline in subjects with and without the APOE e4 allele. Cognitively normal subjects were given the NEO Five Factor Personality Inventory, had APOE genotype testing, and completed a battery of neuropsychological tests ever 1-2 years. One of the components of the NEO Five Factory Personality Inventory is neuroticism. Questions related to neuroticism pertain to depression, anxiety, and anger, which reflect a proneness to stress. Subjects with a high level of neuroticism (clinical cutoff: 56) had a more rapid age-related memory decline, and this effect was more pronounced in APOE e4 carriers.
Differentiating the Logopenic and Nonfluent/Agrammatic Variants of Primary Progressive Aphasia by Selective Word Comprehension Impairment
Collin York, Christopher A. Olm, Sharon Ash, Katya Rascovsky & Murray Grossman
This study aimed to characterize and investigate the basis for selective word class impairment in logopenic variant primary progressive aphasia (lvPPA) and nonfluent/agrammatic variant primary progressive aphasia (naPPA). Although both lvPPA and naPPA have relatively spared single word comprehension, naPPA may have action verb deficits. Subjects in 3 groups (lvPPA, naPPA, healthy controls) were given a two-alternative forced-choice lexical comprehension task. The task included verb triads (half motion verbs, half cognition verbs) and noun triads (half concrete nouns, half abstract nouns). For example, subjects were given a stimulus word such as ‘collect’, and then would have to match it with either ‘gather’ or ‘grab’. Subjects had MR imaging of their brains, which was followed by a voxel-based morphometry analysis of gray matter atrophy and a regression analysis relating motion verb accuracy to gray matter thickness. The authors found that subjects with naPPA performed worse than controls on motion verbs, and their motion verb performance correlated with grammatical comprehension and left inferior frontal atrophy. Subjects with lvPPA performed worse than controls on motion verbs and concrete nouns, and their motion verb performance correlated with category fluency and left inferior temporal and fusiform atrophy. The authors concluded that the impairment of motion verbs in naPPA was due to grammatical impairment as the left inferior frontal region is associated with grammatical processing. They hypothesized that the impairment of motion verbs in lvPPA may be related to the visual representation of motion verb knowledge, as it was associated with visual association cortex in the left inferior temporal and fusiform gyrus.