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Neurodegenerative diseases account for more disability and cost than any other disease category.

Neurodegenerative diseases and their accompanying psychiatric symptoms are among the most devastating disorders, often robbing patients of their dignity, awareness, and ability to conduct life’s most basic daily activities. By most estimates, neurologic diseases account for more disability and cost than any other disease category. Whether through the slow loss of memory and self in Alzheimer’s disease, the crippling loss of motor function in Parkinson’s disease or the change in mood and motivation that often accompanies these conditions; nervous system disorders present an enormous scientific and social challenge.

The brain is the root of our consciousness, emotions, language, memory, and movement, making it a scientific puzzle researchers are struggling to put together.

The brain is a complex organ with discreet and unique neuronal structures. It is the root of our consciousness, emotions, language, memory, and movement, making it a scientific puzzle researchers are still struggling to put together. In recent years scientists have uncovered new insights on the brain thanks to the decoding of the human genome, greater understanding of brain physiology, the application of a systems and circuitry approach, and more precise imaging technologies.

Time is of the essence as an aging population will only increase the burden of neurodegenerative diseases.1 More than 10 million people worldwide are already living with Parkinson’s disease, while another 46 million have Alzheimer’s or related dementias.2,3 By midcentury, these figures could triple.4,5


Neuroscience is at an inflection point. The confluence of new technologies for visualizing brain function, advances in human genetics and personalized medicine, and our understanding of brain cell biology and neural circuitry presents an unprecedented opportunity to understand and treat brain disorders. Today, more than ever, we are able to identify specific patients and what is unique about their underlying biology that is driving their specific constellation of symptoms and disease progression path. Precision medicine is embedded into everything we do, helping us unravel specific clues into how individual patients will benefit from a certain therapy. By better understanding how diseases manifest differently in different individuals, and tailoring potential treatments, we believe we will have greater success in providing meaningful treatment.

Pfizer is seizing opportunities in neuroscience research by mobilizing its industry-leading strengths…

Pfizer is seizing opportunities in neuroscience research by mobilizing its industry-leading strengths in small molecules, antibodies, peptides, vaccines, and other biomolecules. Pfizer’s Neuroscience Research Unit is focused on investigating potential cures and therapies for diseases such as:

Investigating a small molecule that can act as a modulator of dopamine signaling currently in phase 2 of investigation.
We have two programs in phase 1 of investigation, both looking at whether we can modify the progression of Alzheimer's disease; a modulator of gamma-secretase, and a Beta-secretase inhibitor. Both investigational candidates are helping us understand the role of amyloid plaque accumulation in Alzheimer's disease.

Learn more about Pfizer's Research in Parkinson’s Disease

We're working to deepen our understanding of the brain and the central nervous system to treat not just symptoms, but the underlying causes of disease. While there is still a lot of work to do, the momentum is helping Pfizer and the industry at large to progress in neuroscience research.

Working together since 2010, Pfizer's Neuroscience Research Unit and The Michael J. Fox Foundation (MJFF) have developed a strong collaboration built on the shared urgency to find potential therapies to help people living with Parkinson's disease (PD). Our support covers multiple areas of research including:
Parkinson's Progression Markers Initiative (PPMI)
In collaboration with Pfizer and other biotech and pharmaceutical companies, the Foundation's landmark study is collecting invaluable data and biosamples from more than 1,000 participants to investigate biomarkers of the disease and to build a robust database and specimen bank accessible by researchers for complementary PD research in their own labs across the globe.
Parkinson's Disease Education Consortium
Pfizer is supporting the Foundation's patient and caregiver education and engagement efforts toward better health outcomes for the individual and the collective through optimization of specialist care, use of new treatments and participation in clinical research.
Parkinson's Disease Research Tools Consortium
Pfizer is helping generate and characterize preclinical PD research tools that are made available quickly and at low cost to the scientific community.
LRRK2 Industry Consortium
Mutations in the LRRK2 gene are the greatest known genetic contributor to Parkinson's disease. As part of the consortium, Pfizer is sharing resources and helping troubleshoot common problems to speed efforts to move LRRK2 toward therapeutic relevance for patients. Read more
Parkinson’s UK/The Critical Path Institute (C-Path) In early 2016, Pfizer joined six of the world’s largest pharmaceutical companies in a groundbreaking initiative focused on improving clinical trials for Parkinson’s. The consortium, called the Critical Path for Parkinson’s, brings together researchers, drug companies, and regulators with the goal of making clinical trials smarter, underscoring the need for collaboration among industry, academia, and worldwide regulatory agencies to create a more efficient development process. It is a crucial part of efforts to develop new treatments that would work at the earliest stage of Parkinson’s, with the goal of slowing its progression and eventually finding a cure.
IBM Our collaboration with IBM is a first-of-its-kind research collaboration to develop innovative remote monitoring solutions aimed at transforming how clinicians deliver care to patients suffering from Parkinson’s disease. The goal is to set up a system of sensors, mobile devices, and machine learning to provide real-time, around-the-clock disease symptom information to help clinicians and researchers obtain a better understanding of a patient’s disease progression and medication response. This should ultimately help inform treatment decisions and clinical trial design, while also improving the speed at which new therapeutics are developed.
Akili Interactive Labs In January 2014, Pfizer teamed up with Akili to test the ability of Akili's mobile video game-based platform to detect cognitive differences in healthy elderly people at risk of developing Alzheimer's disease, as defined by the presence of amyloid deposits. As part of the agreement, Pfizer has conducted – and successfully concluded – a clinical trial to evaluate the cognitive abilities of 100 healthy elderly subjects with and without the presence of amyloid in their brains over the course of one month of interaction with the platform.

Pfizer Taps IBM for Research Collaboration to Transform Parkinson’s Care

Work with Us

If you’re interested in collaborating with our Neuroscience and Pain research teams, visit our Neuroscience Partnering pages to learn more about the work we are pursuing.


Meet Some of Pfizer’s Neuroscience Researchers

Selected Publications from the Neuroscience Research Unit

Apolipoprotein E4 Domain Interaction Induces Endoplasmic Reticulum Stress and Impairs Astrocyte Function The Journal of Biological Chemistry Zhong N, Ramaswamy G, Weisgraber KH. October 2 2009
Apolipoprotein E4 domain interaction: Synaptic and cognitive deficits in mice Alzheimer's and Dementia - The Journal of the Alzheimer's Association Zhong N, Scearce-Levie K, Ramaswamy G, Weisgraber KH. May 2008
Cloning and Characterization of a Eukaryotic Pantothenate Kinase Gene (panK) from Aspergillus nidulans The Journal of Biological Chemistry Calder RB, Williams RBW, Ramaswamy G, Rock CO, Campbell E, Unkles SE, Kinghorn JR, Jackowski S. January 22 1999
Discovery of the Potent and Selective M1 PAM-Agonist N-[(3R,4S)-3-Hydroxytetrahydro-2H-pyran-4-yl]-5-methyl-4-[4-(1,3-thiazol-4-yl)benzyl]pyridine-2-carboxamide (PF-06767832): Evaluation of Efficacy and Cholinergic Side Effects. Journal of Medicinal Chemistry Davoren JE, Lee CW, Garnsey M, Brodney MA, Cordes J, Dlugolenski K, Edgerton JR, Harris AR, Helal CJ, Jenkinson S1, Kauffman GW, Kenakin TP2, Lazzaro JT, Lotarski SM, Mao Y, Nason DM, Northcott C, Nottebaum L1, O'Neil SV, Pettersen B, Popiolek M, Reinhart V, Salomon-Ferrer R, Steyn SJ, Webb D, Zhang L, Grimwood S. July 1 2016
Effect of domain interaction on apolipoprotein E levels in mouse brain Journal of Neuroscience Ramaswamy G, Xu Q, Huang Y, Weisgraber KH. November 16 2005
First-In-Human safety and long-term exposure data for AAB-003 (PF-05236812) and biomarkers after intravenous infusions of escalating doses in patients with mild to moderate Alzheimer’s disease Alzheimer's Research & Therapy Delnomdedieu M, Duvvuri S, Li DJ, Atassi N, Lu M, Brashear HR, Liu E, Ness S, Kupiec JW. March 1 2016
Inhibition of glucosylceramide synthase stimulates autophagy flux in neurons. Journal of Neurochemistry Shen W, Henry AG, Paumier KL, Li L, Mou K, Dunlop J, Berger Z, Hirst WD. June 2014
Leucine-rich Repeat Kinase 2 (LRRK2) Pharmacological Inhibition Abates α-Synuclein Gene-induced Neurodegeneration. The Journal of Biological Chemistry Daher JP, Abdelmotilib HA, Hu X, Volpicelli-Daley LA, Moehle MS, Fraser KB, Needle E, Chen Y, Steyn SJ, Galatsis P, Hirst WD, West AB. August 7 2015
Olanzapine Treatment of Adolescent Rats Alters Adult D2 Modulation of Cortical Inputs to the Ventral Striatum International Journal of Neuropsychopharmacology Brooks JM, O’Donnell P, Frost DO. October 19 2016
Passive immunotherapy targeting amyloid-β reduces cerebral amyloid angiopathy and improves vascular reactivity. Brain, A Journal of Neurology Bales KR, O'Neill SM, Pozdnyakov N, Pan F, Caouette D, Pi Y, Wood KM, Volfson D, Cirrito JR, Han BH, Johnson AW, Zipfel GJ, Samad TA. October 22 2015
Pathogenic LRRK2 mutations, through increased kinase activity, produce enlarged lysosomes with reduced degradative capacity and increase ATP13A2 expression. Human Molecular Genetics Henry AG, Aghamohammadzadeh S, Samaroo H, Chen Y, Mou K, Needle E, Hirst WD. August 6 2015
PDE4B as a microglia target to reduce neuroinflammation. GLIA Pearse DD, Hughes ZA. April 1 2016
PPARα controls the intracellular coenzyme A concentration via regulation of PANK1α gene expression Journal of Lipid Research The Journal of Biological Chemistry Calder RB, Williams RSB, Ramaswamy G, Rock CO, Campbell E, Unkles SE, Kinghorn JR, Jackowski S. January 2004
Tool compounds robustly increase turnover of an artificial substrate by glucocerebrosidase in human brain lysates. PLoS One Berger Z, Perkins S, Ambroise C, Oborski C, Calabrese M, Noell S, Riddell D, Hirst WD. March 12 2015
1Niccoli T, Partridge L.Ageing as a risk factor for disease.Curr Biol. 2012 Sep 11;22(17):R741-52. doi: 10.1016/j.cub.2012.07.024.
2Parkinson's Disease Foundation. Available on Accessed on August 1, 2016.
3World Alzheimer Report 2015: The Global Impact of Dementia. Alzheimer's Disease International (ADI), London.
4Blennow K, de Leon MJ, Zetterberg H. Alzheimer disease. Lancet. 2006;368(9533):387–403. Waring SC, Rosenberg RN. Genome-wide association studies in Alzheimer disease. Arch Neurol. 2008; 65(3):329–34. Available on Accessed on March 10, 2015.
5Dorsey ER, Constantinescu R, Thompson JP, et al. Projected number of people with Parkinson disease in the most populous nations, 2005 through 2030.Neurology. 2007 Jan 30;68(5):384-6. Epub 2006 Nov 2.