Research Topics
| E D RobersonSummaryAffiliation: University of California Country: USA Publications
Research Grants
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Detail Information
Publications
Frontotemporal dementia progresses to death faster than Alzheimer diseaseE D Roberson
Memory and Aging Center, Department of Neurology, University of California, San Francisco, CA, USA
Neurology 65:719-25. 2005..Frontotemporal lobar degeneration (FTLD) is a common cause of non-Alzheimer dementia, but its natural history and the factors related to mortality in affected patients are not well understood...
Frontotemporal dementiaErik D Roberson
Memory and Aging Center, Department of Neurology, University of California San Francisco, 1650 Owens Street, San Francisco, CA 94158, USA
Curr Neurol Neurosci Rep 6:481-9. 2006....
Reducing endogenous tau ameliorates amyloid beta-induced deficits in an Alzheimer's disease mouse modelErik D Roberson
Gladstone Institute of Neurological Disease, San Francisco, CA 94158, USA
Science 316:750-4. 2007..Thus, tau reduction can block Abeta- and excitotoxin-induced neuronal dysfunction and may represent an effective strategy for treating Alzheimer's disease and related conditions...
Enkephalin elevations contribute to neuronal and behavioral impairments in a transgenic mouse model of Alzheimer's diseaseWilliam J Meilandt
Gladstone Institute of Neurological Disease, San Francisco, California 94158, USA
J Neurosci 28:5007-17. 2008..We conclude that enkephalin elevations may contribute to cognitive impairments in hAPP mice and possibly in humans with AD. The therapeutic potential of reducing enkephalin production or signaling merits further exploration...
Antiamyloidogenic and neuroprotective functions of cathepsin B: implications for Alzheimer's diseaseSarah Mueller-Steiner
Gladstone Institute of Neurological Disease, University of California, San Francisco, 1650 Owens Street, 94158, USA
Neuron 51:703-14. 2006..Thus, CatB likely fulfills antiamyloidogenic and neuroprotective functions. Insufficient CatB activity might promote AD; increasing CatB activity could counteract the neuropathology of this disease...
Abnormal social behaviors in mice lacking Fgf17K Scearce-Levie
Gladstone Institute of Neurological Disease, San Francisco, CA 94158 2261, USA
Genes Brain Behav 7:344-54. 2008..Our findings show that Fgf17 is required for several complex social behaviors and suggest that disturbances in Fgf17 signaling may contribute to neuropsychiatric diseases that affect such behaviors...
Frontotemporal lobar degeneration: demographic characteristics of 353 patientsJulene K Johnson
Department of Neurology, Memory and Aging Center, University of California, San Francisco, 94117, USA
Arch Neurol 62:925-30. 2005..The publication of consensus criteria for FTLD, however, prompted systematic studies. The criteria categorize FTLD into 3 subgroups: frontotemporal dementia, semantic dementia, and progressive nonfluent aphasia...
Aberrant excitatory neuronal activity and compensatory remodeling of inhibitory hippocampal circuits in mouse models of Alzheimer's diseaseJorge J Palop
Gladstone Institute of Neurological Disease, San Francisco, CA 94158, USA
Neuron 55:697-711. 2007..Aberrant increases in network excitability and compensatory inhibitory mechanisms in the hippocampus may contribute to Abeta-induced neurological deficits in hAPP mice and, possibly, also in humans with AD...
100 years and counting: prospects for defeating Alzheimer's diseaseErik D Roberson
Gladstone Institute of Neurological Disease and Department of Neurology, University of California, San Francisco, CA 94158, USA
Science 314:781-4. 2006..The predicted increase in AD cases over the next few decades makes the development of better treatments a matter of utmost importance and urgency...
Research Grants
- Mechanisms for Tau Involvement in Alzheimer's DiseaseERIK ROBERSON; Fiscal Year: 2007..The mentoring and research experience described in this proposal will facilitate the candidate's goal of an independent faculty research position. ..
