Association of amyloid-??  and tau deposition pathology and adultlate-onset
epilepsy in Alzheimer disease
 


   Note: An Official Proposal has not been Submitted to NACC.


   Lead Investigator:    Rohit Marawar
   Institution      :    Wayne State University School of Medicine
   E-Mail           :    ramarawar@med.wayne.edu
   Proposal ID      :    1790



   Proposal Description:
   Experimental Animal studies have supported a role for abnormal protein deposition amyloid-?? in epileptogenesis in Alzheimer?#128#153s disease (AD). More evidence is present for amyloid-beta as compared to tau depostion however clinically onset os seizures is congruent with tau deposition. Here, we proposed the hypothesis that an increased burden of amyloid-?? and/or tau pathology in the brain drive the incidence of epilepsypathogenesis of epilepsy and onset of clinical seizures. , particularly in the context of Alzheimer disease (AD). If AD progression and amyloid-?? accumulation foster the development of adult-onset epilepsy, seizure screen and intervention in late-stage AD is strongly warrantedThis has clinical implicatons as anti-amyloid or tau therapies can help with seizure control. Strategies to slow down amyloid-?? deposition might offer provide extra additional benefits in preventing further neuronal injury.