Posterior Accumulation of Tau and Concordant Hypometabolism in an Early-Onset Alzheimer’s Disease Patient with Presenilin-1 Mutation

Author:

Smith Ruben1,Wibom Moa2,Olsson Tomas3,Hägerström Douglas4,Jögi Jonas5,Rabinovici Gil D.6,Hansson Oskar7

Affiliation:

1. Departments of Neurology, Skåne University Hospital, Lund-Malmö, Sweden

2. Memory Clinic, Ängelholm Hospital, Ängelholm, Sweden

3. Radiation Physics, Skåne University Hospital, Lund-Malmö, Sweden

4. Clinical Neurophysiology, Skåne University Hospital, Lund-Malmö, Sweden

5. Clinical Physiology and Nuclear Medicine, Skåne University Hospital, Lund-Malmö, Sweden

6. Memory and Aging Center, Department of Neurology, University of California, San Francisco, CA, USA

7. Memory clinic, Skåne University Hospital, Lund-Malmö, Sweden

Publisher

IOS Press

Subject

Psychiatry and Mental health,Geriatrics and Gerontology,Clinical Psychology,General Medicine,General Neuroscience

Reference10 articles.

1. The presenilins and Alzheimer’s disease;Hutton;Hum Mol Genet,1997

2. Diverging patterns of amyloid deposition and hypometabolism in clinical variants of probable Alzheimer’s disease;Lehmann;Brain,2013

3. Amyloid burden and metabolic function in early-onset Alzheimer’s disease: Parietal lobe involvement;Ossenkoppele;Brain,2012

4. Early clinical PET imaging results with the novel PHF-tau radioligand [F-18]-T807;Chien;J Alzheimers Dis,2013

5. American Psychiatric Association. Work Group to Revise DSM-III. (1987) Diagnostic and statistical manual of mental disorders: DSM-III-R, American Psychiatric Association, Washington, DC.

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