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Abstract Details

Co-Occurring PSP Pathology in Alzheimer’s Disease: A Case Series
Aging, Dementia, and Behavioral Neurology
Aging and Dementia Posters (7:00 AM-5:00 PM)
025
To describe the clinical and neuropathological features of Alzheimer’s disease (AD) cases with secondary Progressive supranuclear palsy (PSP) neuropathological changes.
Secondary PSP neuropathology in the setting of primary AD is rare.  While AD co-pathology influences clinical phenotypes in certain disorders, it is unknown if PSP co-pathology alters the phenotypes of AD cases or if PSP neuropathology occurs in a different distribution than in primary PSP cases.

Data was collected through the UCSD Alzheimer’s disease research center (UCSD-ADRC). We searched the UCSD-ADRC brain-bank for cases with a clinical diagnosis of probable AD, intermediate/high levels of AD neuropathologic change, and secondary PSP pathology. Diagnostic immunohistochemistry using formalin-fixed paraffin-embedded sections was performed using antibodies directed against tau (PHF-1) and beta-amyloid (ab69d).

Of 1296 cases with primary Alzheimer’s disease pathology, 5 cases (2 women, 3 men) were identified with secondary PSP pathology (0.3%). Age of onset was 72 years (+/-3.8 years) with an 11 year disease duration (+/-2.1 years).  One case had mild parkinsonism and another had a gait disorder arising 5 years post-onset. No cases met NINDS-SPSP criteria for possible or probable PSP. One case would have been ‘suggestive of PSP’ by MDS-PSP criteria.  At autopsy, all cases were Braak AD tau stage III and above.  Tufted astrocytes, globose tangles, and/or coiled bodies were observed in variable amounts in the globus pallidus, striatum, substantia nigra, pons, dentate nuclei of the cerebellum, and frontal cortex. 

AD pathology with PSP co-pathology is a rare occurrence in late onset dementias.  Cases described here would not have met clinical criteria for PSP and have a typical onset and disease duration for AD.  PSP pathology appears to follow similar distribution patterns to primary PSP. Additional immunohistochemistry for 3-repeat (3R), 4-repeat (4R), and AD-specific (GT-38) tau will delineate anatomic distributions of AD and PSP pathology.
Authors/Disclosures
David G. Coughlin, MD (University of California San Diego)
PRESENTER 		Dr. Coughlin has received personal compensation in the range of $500-$4,999 for serving as a Consultant for M3 Global Research. The institution of Dr. Coughlin has received research support from Â鶹´«Ã½Ó³»­. The institution of Dr. Coughlin has received research support from NIA. The institution of Dr. Coughlin has received research support from NINDS.
No disclosure on file
David P. Salmon, PhD (Univ of Calif-San Diego) Dr. Salmon has nothing to disclose.
Douglas Galasko, MD (Dept. of Neurosciences, UCSD) Dr. Galasko has received personal compensation in the range of $5,000-$9,999 for serving as a Consultant for Eisai. Dr. Galasko has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Eli Lilly, Inc. Dr. Galasko has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Roche Diagnostics. Dr. Galasko has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Cognition THeraprutics. Dr. Galasko has received personal compensation in the range of $500-$4,999 for serving on a Scientific Advisory or Data Safety Monitoring board for Artery Therapeutics.
Anne E. Hiniker, MD (University of California, San Francisco) Dr. Hiniker has nothing to disclose.