Sanjay W Pimplikar Ph.D.

Associate Staff

  • Department of Neurosciences
  • Lerner Research Institute
  • 9500 Euclid Avenue
  • Cleveland, Ohio 44195
  • (216) 444-9513
  • (216) 444-7927

Alzheimer's disease (AD) is the most common cause of dementia worldwide. The cause of the disease is not completely understood and currently there is no cure for AD. Genetic and cell biological studies show that amyloid precursor protein (APP) is intimately associated with AD pathogenesis. We generated a transgenic mice expressing a small fragment of APP called AICD and demonstrated that AICD-Tg mice develop major AD-like pathologies such as tau tangles, neurodegeneration, neuroinflammation and loss of memory.


In the past year we have focused on understanding the basis of memory loss in AICD-Tg mice. Towards this goal, we examined the brains electrophysiologically and showed that they were deficient in long-term potentiation (LTP). We also performed ultrastructural studies using 3-D electron microscopy and found that AICD-Tg mice exhibit smaller and fewer synapses compared wild-type controls. These findings provide structural and functional basis for memory loss in AICD-Tg mice.


We are currently exploring the contribution of neuroinflammation to AD-pathologies and memory loss. It is known that chronic neuroinflammation and inflammatory cytokines inhibit synaptic communication and lead to axonal loss and neuronal death. We previously showed that anti-inflammatory treatments prevent AD-pathologies in AICD-Tg mice. We are currently collaborating with a biotech company to study the efficacy of stem cells against AD. We are also examining the efficacy of drugs targeted towards Tau in rescuing AD-associated memory loss. Our future goals are aimed at developing and validating alternative therapeutic strategies against AD since amyloid-lowering therapies have not been successful.


In other words ...

No explanation available.

1. Lifelong management of amyloid-beta metabolism to prevent Alzheimer’s disease. Pimplikar SW. N Engl J Med 2012 (in press).


2. The Apolipoprotein-E-Mimetic COG112 Protects Amyloid Precursor Protein Intracellular Domain-Overexpressing Animals from Alzheimer's Disease-Like Pathological Features.

Ghosal K, Stathopoulos A, Thomas D, Phenis D, Vitek MP, Pimplikar SW.

Neurodegener Dis. 2012 Sep 7. [Epub ahead of print]


3. Knockdown of amyloid precursor protein in zebrafish causes defects in motor axon outgrowth.

Song P, Pimplikar SW.

PLoS One. 2012;7(4):e34209. Epub 2012 Apr 24.


4. Amyloid precursor protein: more than just neurodegeneration.

Pimplikar SW, Ghosal K.

Stem Cell Res Ther. 2011 Oct 14;2(5):39. doi: 10.1186/scrt80.