Sreeganga Chandra, PhD

Associate Professor of Neurology and Neuroscience; Associate Professor, Neurology; Associate Professor of Neuroscience; Deputy Chair of Neuroscience

Research Departments & Organizations

Neurology: Chandra Lab

Interdepartmental Neuroscience Program

Kavli Institute for Neuroscience

Program in Cellular Neuroscience, Neurodegeneration and Repair

Yale Stem Cell Center

Research Interests

Neurodegenerative Diseases; Neurology; Neuronal Ceroid-Lipofuscinoses; Parkinson Disease; Receptors, Presynaptic; Synapses

Research Summary

My lab explores two related themes, those of synapse loss and neurodegeneration. Synapse loss is an early, defining event in neurodegenerative diseases, such as Parkinson's disease. In these prolonged diseases, decreases in synapse density are the best correlates of disease progression.Yet, little is known about the pathways that maintain synapses and their roles in aging and neurodegeneration. We are characterizing familial neurodegeneration genes that encode synaptic proteins to understand this important step in disease pathogenesis. Our lab uses mouse models as well as iPSC derived neuronal models in combination with biochemical, cell biological  and in vivo approaches to tackle these important questions.

Specialized Terms:

  • Presynaptic Biology
  • Synapse Maintenance
  • Parkinson's Disease
  • Neuronal Ceroid Lipofuscinosis
  • Neurodegeneration

Extensive Research Description

  • Role of the endolysosomal pathway in Parkinson's disease
  • Protein palmitoylation and neuronal ceroid lipofuscinosis
  • Identification of the physiological function of synucleins
  • Role of CSP alpha in synapse maintenance
  • Identification of novel synapse maintenance genes

Selected Publications

See list of PubMed publications

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Contact Info

Sreeganga Chandra, PhD
Mailing Address
295 Congress Avenue

New Haven, CT 06536

Chandra Lab

Research Image 1

Many genes in the endolysosomal pathway are genetically linked to Parkinson's disease. We are investigating several genes that function in synaptic vesicle endocytosis.

Research Image 2

Synuclein null synapses showing a deficit in HRP-cholera toxin positive vesicles (black vesicles). This experiment in synuclein null neurons supports a physiological role for alpha-synuclein in synaptic vesicle endocytosis.