There is significant clinical heterogeneity in clinical phenotypes even within classical neurodegenerative disease categories of Alzheimer’s disease, Fronto-temporal dementia, Lewy body dementia etc. Clinical phenotypes include differences in predominant symptoms (e.g., language, behavior, judgment, neuropsychiatric, memory) and differences in rate of progression and outcomes. It is increasingly recognized that there are underlying differences in genetic and molecular pathologies that drive the differences in these clinical phenotypes. Understanding this in detail is key to providing future precision medicine therapies targeting chronic neurodegenerative diseases.

Mapping the interrelationships between the underlying molecular changes to clinical phenotype is informed by bioinformatics and novel data analysis methods that take insights from clinical medicine, cognitive neuroscience, neuroimaging, genetic and transcriptomic data, protein biomarkers, and neuropathology to uncover key drivers.

Using these tools, we aim to: 1) develop clinical biomarkers to predict outcomes of interest in neurodegenerative diseases, and 2) develop precision medicine therapies targeting key pathological drivers.

Contact Information:

Jagan Pillai, MD, PhD

Funding Sources:

Alzheimer’s Association

Cleveland Brain Health Foundation

Keep Memory Alive Foundation

National Institute of Aging

Members & Collaborations

Members & Collaborations

Cleveland Clinic Affiliations

  • Lynn Bekris, PhD (Genomics Institute, Cleveland Clinic)
  • Cornelia Bergmann, PhD (Department of Neurosciences, Cleveland Clinic)

External Relationships & Collaborations

  • Gurkan Bebek, PhD (Case Western Reserve, Center for Proteomics and Bioinformatics)
  • Mark Chance, PhD (Case Western Reserve, Center for Proteomics and Bioinformatics)
  • Masaru Miyagi, PhD (Case Western Reserve, Department of Pharmacology)
  • Xinglong Wang, PhD (Case Western Reserve, Department of Pathology)


Key Inflammatory Pathway Activations in the MCI Stage of Alzheimer’s Disease. Pillai JA, Maxwell S, Bena J, Bekris, LM, Rao, SM, Chance M, Lamb BT, Leverenz JB, for the Alzheimer ’s Disease Neuroimaging Initiative* Ann Clin Transl Neurol. 2019 Jul;6(7):1248-1262.

Highly elevated cerebrospinal fluid total tau level reflects higher likelihood of non-amnestic subtype of Alzheimer’s disease. Pillai JA, Bonner-Jackson A, Bekris, LM, Safar, J, Bena J, Leverenz JB. J Alzheimers Dis. 2019;70(4):1051-1058.

Amygdala Sign, a FDG-PET signature of Dementia with Lewy Bodies. Parkinsonism Relat Disord. Pillai JA, Wu G, Tousi, B, Larvie M, Leger G, Leverenz J. 2019 Jul;64:300-303.

Rapidly Progressive Alzheimer's Disease in Two Distinct Autopsy Cohorts. Pillai JA, Appleby BS, Safar J, Leverenz JB. J Alzheimers Dis. 2018;64(3):973-980.

Lack of Accurate Self-appraisal is Equally Likely in MCI from Parkinson's Disease and Alzheimer's Disease. Pillai JA, Bonner-Jackson A, Floden D, Fernandez H, Leverenz JB. Mov Disord Clin Pract. 2018 Mar 23;5(3):283-289.

Impact of Alzheimer's Disease, Lewy Body and Vascular Co-Pathologies on Clinical Transition to Dementia in a National Autopsy Cohort. Pillai JA, Butler RS, Bonner-Jackson A, Leverenz JB. Dement Geriatr Cogn Disord. 2016;42(1-2):106-16.