Anne B. Young

Last updated
Anne Buckingham Young
Anne B Young.jpg
Born
Evanston, Illinois
Alma mater Vassar College, Johns Hopkins University School of Medicine
Known for Neurodegenerative diseases, Huntington's disease, Glutamate
SpousesJohn B. Penney, Jr. (1971–1999), Stetson Ames (2005–present)
Scientific career
Fields Neuroscience
Institutions University of Michigan, Harvard Medical School, Massachusetts General Hospital
Doctoral advisor Solomon H. Snyder

Anne Buckingham Young is an American physician and neuroscientist who has made major contributions to the study of neurodegenerative diseases, with a focus on movement disorders like Huntington's disease and Parkinson's disease. Young completed her undergraduate studies at Vassar College and earned a dual MD/PhD from Johns Hopkins Medical School. She has held faculty positions at University of Michigan and Harvard University. [1] She became the first female chief of service at Massachusetts General Hospital when she was appointed Chief of Neurology in 1991. She retired from this role and from clinical service in 2012. She is a member of many academic societies and has won numerous awards. Young is also the only person to have been president of both the international Society for Neuroscience and the American Neurological Association. [2]

Contents

Early and personal life

Young grew up in Evanston, a suburb located on the North Shore of Chicago. Growing up, her feisty nature earned her the nickname of "Tiger Annie" among friends and family. As a result, she was sent to prep school to keep her out of trouble. [3] Both of Young's parents were involved in science; her father studied chemistry at Harvard, and her mother studied physics at Vassar College. [4]

After receiving her undergraduate degree from Vassar College, Young enrolled in an MD/PhD Program at Johns Hopkins Medical School. There, she met her first husband, John (Jack) B. Penney Jr. Throughout their marriage, they collaborated professionally and together had two daughters, Jessica and Ellen. Penney died suddenly in 1999. Young is currently married to her high school boyfriend Stetson Ames. [4]

Throughout her life, Young has had trouble reading due to dyslexia. After Penney's death, Young also struggled with depression and was diagnosed with bipolar disorder for which she receives therapy. She continued to run the department of neurology at Massachusetts General Hospital. [5]

Professional career

Overview

Young's research career includes many highlights. In 1974 she published a paper contributing to the discovery of glutamate as a neurotransmitter. [6] Additionally, a 1989 paper she co-authored describing an anatomically and pharmacologically derived model of basal ganglia disorders has been cited over 5000 times. [7] As part of the Huntington Study Group, Young has published multiple reviews about the progress of research on Huntington's Disease. Additionally, she participated in an assessment of the Unified Huntington's Disease Rating Scale, which has been cited over 1000 times. [8] [9] [10] [11] [12]

She received a BA in chemistry from Vassar College. Young was then awarded both an M.D. and Ph.D. in Pharmacology from Johns Hopkins within 5 years. [3] Her dissertation work was in a neuropharmacology lab focused on psychiatric disorders. Their group helped to define the role of neurotransmitters in different cell types. [4] [6] She completed residency training in neurology at the University of California San Francisco. With her late husband John B. Penney Jr., Young started a laboratory at the University of Michigan studying the anatomy and pharmacology of the basal ganglia. [13] In 1991, Young was appointed chief of neurology at Massachusetts General Hospital and the Julianne Dorn Professor of Neurology at Harvard Medical School. She was the first female service chief in the hospital's 180-year history. [3] She and Penney developed the Mass General Institute for Neurodegenerative Disease, a collaborative location to streamline the process of research and clinical treatment development. [14] Throughout her career, Young participated in the Venezuela Huntington's Disease Project with Nancy Wexler. [4] Young was the president of the Society for Neuroscience from 2003 to 2004 and of the American Neurological Association from 2003 to 2005.

Vassar College - undergraduate studies

Young completed her undergraduate studies summa cum laude at Vassar College, with a major in chemistry and minors in art history and philosophy. She worked in a laboratory there, developing an interest in biochemistry under her professor, Anne Gounaris. [4] Together, they analyzed pyruvate decarboxylase, an enzyme involved in metabolism. An assay technique developed by Young is published in a paper in the Journal of Biological Chemistry. [15]

Johns Hopkins Medical School

After graduating from Vassar, Young enrolled in Johns Hopkins Medical School. Young was one of nine women in her class of 110. In an autobiography, Young describes how her lectures had mostly male professors and students. They would show nude photos of women for entertainment. She once switched one of the photos with a nude picture of a man to embarrass the lecturer. Young also met her husband Jack during her first year, and they continued their relationship while both pursuing careers in neurology. [4]

Young spent only two and a half years completing her required medical school courses and clerkships. During the PhD portion of her graduate studies, Young worked with Professor Solomon Snyder on preliminary analyses of potential neurotransmitters, such as glutamate, glycine, and GABA. Data provided by Young was the first suggestion that glutamate was a neurotransmitter of cerebellar granule cells. [6] Young also worked with glycine and GABA receptors and found a way to detect inhibitory amino acid receptors using neurotoxins. [4] Young developed several collaborative projects with others in the neurology department at Johns Hopkins. She graduated with her MD in 1973 and her PhD in pharmacology in 1974 with ten publications under her belt. [1]

UCSF - internship and residency

Young applied for internship and residency programs at University of California, San Francisco (UCSF). She was accepted to the UCSF residency program and matched with an internship at nearby Mt. Zion Hospital in 1974. Young completed her residency a year behind her husband, Jack, and became pregnant during her second year. [4] In her third year, she was chosen as chief resident. [4] After completing their residencies, the couple found jobs at the University of Michigan and began in 1978. [4]

University of Michigan

Mentored by the head of neurology, Sid Gilman, Young began to write grants and to work on positron emission tomography studies of Huntington's Disease. [4] Young wrote her first grant during residency and decided to focus on spinal cord spasticity. Her grant received funding from the National Institute of Neurological Disorders and Stroke. [16] Later that year, Young gave birth to her second daughter. [4]

Young and her husband partnered in all of their research and clinical work. They established the U of M Movement Disorders Clinic. [13] The couple took on specific roles. Young was the expert in pharmacology, neurotransmitters, and receptors. In the clinic, she focused on hyperkinetic disorders like Huntington's and Tourette's syndrome. Penney was the expert in stereotactic surgery, anatomy, computer programs, and statistics. In the clinic, he focused on hypokinetic movement disorders like Parkinson's. [4] The couple pioneered research on the basal ganglia's involvement in these movement disorders. Their research identified a pathway in the cortex that acts on striatal cells (circuits through the cortex/striatum/pallium/subthalamic nucleus/substantia nigra/thalamus and back to the cortex.) This circuit was predicted to be defective in both Huntington's and Parkinson's patients. They published their theory in 1986 in Movement Disorders and continued to investigate the problem with Dr. Roger L. Albin. The evidence and the hypothesis from their publication led to the development of deep brain stimulation, a treatment for Parkinson's Disease. [3] In 1989, they published their work proposing a new model of the basal ganglia's involvement in Huntington's and Parkinson's in Trends in Neuroscience . [17] Albin now occupies a faculty position at University of Michigan which is named in her honor: the Anne B. Young Collegiate Professor of Neurology. [18]

Venezuela Huntington's disease project

In 1981, Young traveled with Nancy Wexler to Lake Maracaibo to study a family of many members with or at risk of Huntington's disease. She and her husband returned yearly with Wexler to examine members of the family, to take DNA samples, and to develop a detailed pedigree. [3] For 22 years, the team continued to travel to Venezuela until international relations with Hugo Chávez halted the project. [19] Their work in Venezuela contributed to Jim Gusella's discovery of the location of the gene that causes Huntington's disease. [3] Ten years later, a collaborative group isolated the gene and the mutation which causes Huntington's. This discovery led to the development of genetic testing for at-risk individuals, allowing them and clinical researchers to know whether they would develop Huntington's disease. [12]

Massachusetts General Hospital

In 1991, Young was recruited and appointed to chief of neurology at Massachusetts General Hospital (MGH). She was the first female chief in the hospital's history and the first female chief of neurology at a teaching hospital in the United States. [20]

MassGeneral Institute for Neurodegenerative Diseases (MIND)

As chief of neurology, Young recognized the potential benefit of bringing together the existing labs at MGH studying neurodegenerative diseases. She developed a proposal to convert a nearby Navy building into an open lab space for the study of neurodegenerative disease, and she brought this to hospital administrators. Her proposal received funding, and she was given almost an entire building where the Mass General Institute for Neurodegenerative Disease (MIND) was established. MIND seeks to have a broad focus to study not only the cause of these diseases, but also to develop effective therapeutic techniques. Another aspect of MIND Young helped to foster is collaborative teamwork between researchers. MIND has made many contributions to research of neurodegenerative diseases, including a role in the development of several clinically proven therapies. [14]

Anne B. Young Translational Medicine Fellowship

The Massachusetts General Hospital Department of Neurology partnered with Biogen to offer a fellowship in Young's honor. The fellowship trains fellows to quickly and efficiently perform research and create treatments for neurological disorders. The fellowship is focused on scientists early in their careers to create a combined focus on academia and industry. [2]

Harvard Medical School

In 1991, Young began as chief of neurology at Mass Gen and professor of neurology at Harvard Medical School. In 2012, she was appointed Distinguished Julieanne Dorn Distinguished Professor of Neurology, where she teaches presently. Her research has been in metabotropic glutamate receptors in neurodegeneration and Alzheimer's disease. In 2004, she mentored a student project about the gene for Huntington's Disease, which codes for the protein huntingtin. Since 2012, she has given up her lab in order to fundraise and let others have access to her prior space and resources. [3] [21]

American Neurological Association

In 2001, Young was the second female chosen to be president of the American Neurological Association. [3] During Young's tenure, a mentoring program for neurologists and neuroscientists was developed through a partnership with NINDS. This program continues today. [4] [22]

Society for Neuroscience

In 2003, Young was elected president of the Society for Neuroscience. [4] During Young's tenure, she oversaw the design and development of a new headquarters building for the Society in Washington D.C. The building was designed to be as environmentally friendly as possible. [23] She has also served as chair of the Government and Public Affairs Committee for the Society. [24]

Selected publications

Over her many years in research, Young has made contributions to the study of neuroscience. She has been credited in over a hundred publications, with a majority of contributions focusing on neurodegenerative diseases. [21] Following is a chronologically organized list of a selection of Young's papers which presented significant findings at that time in the field.

This paper showed that histamine in neonatal brains is concentrated in the nucleus, suggesting a role for histamine in brain development. [25]

Glutamic Acid Glutamic acid test.svg
Glutamic Acid

This paper correlated the loss of the excitatory action of granule cells and the selective loss of synaptic glutamic acid, [26] to suggest glutamate as the possible primary neurotransmitter of the granule cell. Today glutamate is considered to be the chief excitatory neurotransmitter in the human central nervous system. [6]

After further studies solidified glutamic acid as a critical excitatory neurotransmitter involved in the formation of memory and in learning, Young and her team hypothesized on potential ramifications of dysfunctioning glutamic acid. [27] Their research linked the potential harmful and toxic effects of glutamic acid in Alzheimer's disease. [28]

In this paper, Young and her colleagues investigated the degeneration of striatal projection neurons, present in the basal ganglia in the brain. Using immunohistochemistry, the progression of Huntington's Disease was imaged and tracked to identify how the disease reduces the number of neurons in the striatum. [29]

This paper described a model of basal ganglia disorders, including hyperkinetic and hypokinetic disorders. Through different physical and systems-based research, models of neural networks of Early Stage Huntington's Disease and Parkinson's Disease were proposed. The models suggest that different areas of the striatum, previously established as the area of the brain most directly related to the diseases, may be involved in the different steps and features of motor control. [7] This discovery allowed researchers to pursue research focused on the different areas and types of degradation of the striatum correlated with either Parkinson's or Huntington's disease. [17]

In this paper, Young and her co-author Greenamyre present research on the role of disrupting different excitatory amino acid mechanisms in the hippocampus and cerebral cortex of the brain. They concluded that disrupting these pathways could play a role in both the development of symptoms of Alzheimer's disease, specifically in memory loss, and the pathological symptoms, or physical changes in the brain. [30]

Colleagues

Awards and honors

In 1994, Young was chosen as a member of the Institute of Medicine. [32] She was elected to the American Academy of Arts and Sciences in 1995. [33] In 1999, Young was awarded the Dean's Award for Support and Advancement of Women Faculty by Harvard Medical School. [34] Two years later, Young won the Marion Spencer Fay Award, which recognizes excellence in medicine and science through innovation and leadership. [35] In 2005, she was granted fellowship to the Royal College of Physicians, England. In 2006, she received the Milton Wexler Award from the Hereditary Disease Foundation. Young has also been given two distinguished alumni awards, one from Johns Hopkins Medical School and one from Vassar College. [36] She holds a distinguished professor position at Harvard, the Julieanne Dorn Professor of Neurology. [1]

Related Research Articles

Neurochemistry is the study of chemicals, including neurotransmitters and other molecules such as psychopharmaceuticals and neuropeptides, that control and influence the physiology of the nervous system. This particular field within neuroscience examines how neurochemicals influence the operation of neurons, synapses, and neural networks. Neurochemists analyze the biochemistry and molecular biology of organic compounds in the nervous system, and their roles in such neural processes including cortical plasticity, neurogenesis, and neural differentiation.

<span class="mw-page-title-main">Excitatory synapse</span> Sort of synapse

An excitatory synapse is a synapse in which an action potential in a presynaptic neuron increases the probability of an action potential occurring in a postsynaptic cell. Neurons form networks through which nerve impulses travels, each neuron often making numerous connections with other cells of neurons. These electrical signals may be excitatory or inhibitory, and, if the total of excitatory influences exceeds that of the inhibitory influences, the neuron will generate a new action potential at its axon hillock, thus transmitting the information to yet another cell.

<span class="mw-page-title-main">Excitotoxicity</span> Process that kills nerve cells

In excitotoxicity, nerve cells suffer damage or death when the levels of otherwise necessary and safe neurotransmitters such as glutamate become pathologically high, resulting in excessive stimulation of receptors. For example, when glutamate receptors such as the NMDA receptor or AMPA receptor encounter excessive levels of the excitatory neurotransmitter, glutamate, significant neuronal damage might ensue. Excess glutamate allows high levels of calcium ions (Ca2+) to enter the cell. Ca2+ influx into cells activates a number of enzymes, including phospholipases, endonucleases, and proteases such as calpain. These enzymes go on to damage cell structures such as components of the cytoskeleton, membrane, and DNA. In evolved, complex adaptive systems such as biological life it must be understood that mechanisms are rarely, if ever, simplistically direct. For example, NMDA in subtoxic amounts induces neuronal survival of otherwise toxic levels of glutamate.

Molecular neuroscience is a branch of neuroscience that observes concepts in molecular biology applied to the nervous systems of animals. The scope of this subject covers topics such as molecular neuroanatomy, mechanisms of molecular signaling in the nervous system, the effects of genetics and epigenetics on neuronal development, and the molecular basis for neuroplasticity and neurodegenerative diseases. As with molecular biology, molecular neuroscience is a relatively new field that is considerably dynamic.

<span class="mw-page-title-main">Hypokinesia</span> Decreased movement due to basal ganglia dysfunction

Hypokinesia is one of the classifications of movement disorders, and refers to decreased bodily movement. Hypokinesia is characterized by a partial or complete loss of muscle movement due to a disruption in the basal ganglia. Hypokinesia is a symptom of Parkinson's disease shown as muscle rigidity and an inability to produce movement. It is also associated with mental health disorders and prolonged inactivity due to illness, amongst other diseases.

<span class="mw-page-title-main">Neuroprotection</span> Relative preservation of neuronal structure and/or function

Neuroprotection refers to the relative preservation of neuronal structure and/or function. In the case of an ongoing insult the relative preservation of neuronal integrity implies a reduction in the rate of neuronal loss over time, which can be expressed as a differential equation. It is a widely explored treatment option for many central nervous system (CNS) disorders including neurodegenerative diseases, stroke, traumatic brain injury, spinal cord injury, and acute management of neurotoxin consumption. Neuroprotection aims to prevent or slow disease progression and secondary injuries by halting or at least slowing the loss of neurons. Despite differences in symptoms or injuries associated with CNS disorders, many of the mechanisms behind neurodegeneration are the same. Common mechanisms of neuronal injury include decreased delivery of oxygen and glucose to the brain, energy failure, increased levels in oxidative stress, mitochondrial dysfunction, excitotoxicity, inflammatory changes, iron accumulation, and protein aggregation. Of these mechanisms, neuroprotective treatments often target oxidative stress and excitotoxicity—both of which are highly associated with CNS disorders. Not only can oxidative stress and excitotoxicity trigger neuron cell death but when combined they have synergistic effects that cause even more degradation than on their own. Thus limiting excitotoxicity and oxidative stress is a very important aspect of neuroprotection. Common neuroprotective treatments are glutamate antagonists and antioxidants, which aim to limit excitotoxicity and oxidative stress respectively.

<span class="mw-page-title-main">Kainic acid</span> Chemical compound

Kainic acid, or kainate, is an acid that naturally occurs in some seaweed. Kainic acid is a potent neuroexcitatory amino acid agonist that acts by activating receptors for glutamate, the principal excitatory neurotransmitter in the central nervous system. Glutamate is produced by the cell's metabolic processes and there are four major classifications of glutamate receptors: NMDA receptors, AMPA receptors, kainate receptors, and the metabotropic glutamate receptors. Kainic acid is an agonist for kainate receptors, a type of ionotropic glutamate receptor. Kainate receptors likely control a sodium channel that produces excitatory postsynaptic potentials (EPSPs) when glutamate binds.

<span class="mw-page-title-main">Glutamate receptor</span> Cell-surface proteins that bind glutamate and trigger changes which influence the behavior of cells

Glutamate receptors are synaptic and non synaptic receptors located primarily on the membranes of neuronal and glial cells. Glutamate is abundant in the human body, but particularly in the nervous system and especially prominent in the human brain where it is the body's most prominent neurotransmitter, the brain's main excitatory neurotransmitter, and also the precursor for GABA, the brain's main inhibitory neurotransmitter. Glutamate receptors are responsible for the glutamate-mediated postsynaptic excitation of neural cells, and are important for neural communication, memory formation, learning, and regulation.

Glutamate transporters are a family of neurotransmitter transporter proteins that move glutamate – the principal excitatory neurotransmitter – across a membrane. The family of glutamate transporters is composed of two primary subclasses: the excitatory amino acid transporter (EAAT) family and vesicular glutamate transporter (VGLUT) family. In the brain, EAATs remove glutamate from the synaptic cleft and extrasynaptic sites via glutamate reuptake into glial cells and neurons, while VGLUTs move glutamate from the cell cytoplasm into synaptic vesicles. Glutamate transporters also transport aspartate and are present in virtually all peripheral tissues, including the heart, liver, testes, and bone. They exhibit stereoselectivity for L-glutamate but transport both L-aspartate and D-aspartate.

<span class="mw-page-title-main">Neurodegenerative disease</span> Central nervous system disease

A neurodegenerative disease is caused by the progressive loss of structure or function of neurons, in the process known as neurodegeneration. Such neuronal damage may ultimately involve cell death. Neurodegenerative diseases include amyotrophic lateral sclerosis, multiple sclerosis, Parkinson's disease, Alzheimer's disease, Huntington's disease, multiple system atrophy, tauopathies, and prion diseases. Neurodegeneration can be found in the brain at many different levels of neuronal circuitry, ranging from molecular to systemic. Because there is no known way to reverse the progressive degeneration of neurons, these diseases are considered to be incurable; however research has shown that the two major contributing factors to neurodegeneration are oxidative stress and inflammation. Biomedical research has revealed many similarities between these diseases at the subcellular level, including atypical protein assemblies and induced cell death. These similarities suggest that therapeutic advances against one neurodegenerative disease might ameliorate other diseases as well.

<span class="mw-page-title-main">Quisqualic acid</span> Chemical compound

Quisqualic acid is an agonist of the AMPA, kainate, and group I metabotropic glutamate receptors. It is one of the most potent AMPA receptor agonists known. It causes excitotoxicity and is used in neuroscience to selectively destroy neurons in the brain or spinal cord. Quisqualic acid occurs naturally in the seeds of Quisqualis species.

<span class="mw-page-title-main">Quinolinic acid</span> Dicarboxylic acid with pyridine backbone

Quinolinic acid, also known as pyridine-2,3-dicarboxylic acid, is a dicarboxylic acid with a pyridine backbone. It is a colorless solid. It is the biosynthetic precursor to niacin.

<span class="mw-page-title-main">Ann Graybiel</span> American neuroscientist

Ann Martin Graybiel is an Institute Professor and a faculty member in the Department of Brain and Cognitive Sciences at the Massachusetts Institute of Technology. She is also an investigator at the McGovern Institute for Brain Research. She is an expert on the basal ganglia and the neurophysiology of habit formation, implicit learning, and her work is relevant to Parkinson's disease, Huntington's disease, obsessive–compulsive disorder, substance abuse and other disorders that affect the basal ganglia.

<span class="mw-page-title-main">Clinical neurochemistry</span>

Clinical neurochemistry is the field of neurological biochemistry which relates biochemical phenomena to clinical symptomatic manifestations in humans. While neurochemistry is mostly associated with the effects of neurotransmitters and similarly functioning chemicals on neurons themselves, clinical neurochemistry relates these phenomena to system-wide symptoms. Clinical neurochemistry is related to neurogenesis, neuromodulation, neuroplasticity, neuroendocrinology, and neuroimmunology in the context of associating neurological findings at both lower and higher level organismal functions.

Translational neuroscience is the field of study which applies neuroscience research to translate or develop into clinical applications and novel therapies for nervous system disorders. The field encompasses areas such as deep brain stimulation, brain machine interfaces, neurorehabilitation and the development of devices for the sensory nervous system such as the use of auditory implants, retinal implants, and electronic skins.

<span class="mw-page-title-main">Glutamate (neurotransmitter)</span> Anion of glutamic acid in its role as a neurotransmitter

In neuroscience, glutamate is the anion of glutamic acid in its role as a neurotransmitter. It is by a wide margin the most abundant excitatory neurotransmitter in the vertebrate nervous system. It is used by every major excitatory function in the vertebrate brain, accounting in total for well over 90% of the synaptic connections in the human brain. It also serves as the primary neurotransmitter for some localized brain regions, such as cerebellum granule cells.

Stephen F. Heinemann (1939–2014) was a professor of neuroscience at the Salk Institute. He was an early researcher in the field of molecular neuroscience, contributing to the current knowledge of how nerves communicate with each other, and the role of neurotransmitters. Stephen Heinemann died August 6, 2014, of kidney failure.

Joseph Thomas Coyle Jr. is an American psychiatrist and neuroscientist. He is the Eben S. Draper Professor of Psychiatry and Neuroscience at Harvard Medical School.

<span class="mw-page-title-main">Willardiine</span> Chemical compound

Willardiine (correctly spelled with two successive i's) or (S)-1-(2-amino-2-carboxyethyl)pyrimidine-2,4-dione is a chemical compound that occurs naturally in the seeds of Mariosousa willardiana and Acacia sensu lato. The seedlings of these plants contain enzymes capable of complex chemical substitutions that result in the formation of free amino acids (See:#Synthesis). Willardiine is frequently studied for its function in higher level plants. Additionally, many derivates of willardiine are researched for their potential in pharmaceutical development. Willardiine was first discovered in 1959 by R. Gmelin, when he isolated several free, non-protein amino acids from Acacia willardiana (another name for Mariosousa willardiana) when he was studying how these families of plants synthesize uracilyalanines. A related compound, Isowillardiine, was concurrently isolated by a different group, and it was discovered that the two compounds had different structural and functional properties. Subsequent research on willardiine has focused on the functional significance of different substitutions at the nitrogen group and the development of analogs of willardiine with different pharmacokinetic properties. In general, Willardiine is the one of the first compounds studied in which slight changes to molecular structure result in compounds with significantly different pharmacokinetic properties.

Ana Cristina Rego is a Portuguese neurologist. She is a professor at the University of Coimbra in Portugal and is head of the research group on Mitochondria and Neurodegenerative disorders, researching on topics such as Alzheimer's disease, Huntingdon's disease, and Parkinson's disease. She is presently president of the Portuguese Society of Neuroscience.

References

  1. 1 2 3 "Anne B. Young, MD, PhD". The Michael J. Fox Foundation for Parkinson's Research. Retrieved February 20, 2020.
  2. 1 2 "Anne B. Young Translational Neuroscience Fellowship". Massachusetts General Hospital. Retrieved February 20, 2020.
  3. 1 2 3 4 5 6 7 8 9 Thomas, Patricia (May 2002). "Brainy Women: At the frontiers of neuroscience". Harvard Magazine. Retrieved February 20, 2020.
  4. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 Buckingham Young, Anne (April 17, 2014). "Anne Buckingham Young". Society for Neuroscience. Retrieved February 20, 2020.
  5. ↑ de Lore, Clare (January 23, 2017). "Neuroscientist Anne Young: 'Trump is not a person I can support in any way'". Noted. Retrieved February 20, 2020.
  6. 1 2 3 4 Fonnum, Frode (1984). "Glutamate: A Neurotransmitter in Mammalian Brain". Journal of Neurochemistry. 42 (1): 1–11. doi:10.1111/j.1471-4159.1984.tb09689.x. PMID   6139418. S2CID   1358914.
  7. 1 2 Albin, Roger L.; Young, Anne B.; Penney, John B. (January 1, 1989). "The functional anatomy of basal ganglia disorders". Trends in Neurosciences. 12 (10): 366–375. doi:10.1016/0166-2236(89)90074-x. hdl: 2027.42/28186 . PMID   2479133. S2CID   8112392.
  8. ↑ Young, Anne B. (October 14, 2009). "Four Decades of Neurodegenerative Disease Research: How Far We Have Come!". The Journal of Neuroscience. 29 (41): 12722–12728. doi:10.1523/JNEUROSCI.3767-09.2009. PMC   2807668 . PMID   19828782 – via PMC.
  9. ↑ Kieburtz, Karl; Penney, John B.; Corno, Peter; Ranen, Neal; Shoulson, Ira; Feigin, Andrew; Abwender, Davi; Greenarnyre, J. Timothy; Higgins, Donald; Marshall, Frederick J.; Goldstein, Joshua (2001-02-27). "Unified huntington's disease rating scale: Reliability and consistency". Movement Disorders. 11 (2): 136–142. doi:10.1002/mds.870110204. ISSN   0028-3878. PMID   11222787. S2CID   45982731.
  10. ↑ Young, Anne B. (February 1, 2003). "Huntingtin in health and disease". The Journal of Clinical Investigation. 111 (3): 299–302. doi:10.1172/JCI17742. PMC   151871 . PMID   12569151 – via PMC.
  11. ↑ Tippett, Lynette J.; Waldvogel, HJ; Snell, Russell G.; Vonsattel, Jean Paul G.; Young, Anne B.; Faull, Richard L. M. (2017). "The Complexity of Clinical Huntington's Disease: Developments in Molecular Genetics, Neuropathology and Neuroimaging Biomarkers". Neurodegenerative Diseases. Advances in Neurobiology. Vol. 15. pp. 129–161. doi:10.1007/978-3-319-57193-5_5. ISBN   978-3-319-57191-1. PMID   28674980.
  12. 1 2 Shoulson, Ira; Young, Anne B. (May 2011). "Milestones in huntington disease". Movement Disorders. 26 (6): 1127–1133. doi:10.1002/mds.23685. PMID   21626556. S2CID   16200136.
  13. 1 2 The University Record (February 22, 1999). "Obituaries: John B. Penney Jr". The University Record. Retrieved March 29, 2020.
  14. 1 2 "Vision". Massachusetts General Hospital: MassGeneral Institute for Neurodegenerative Disease. 2014. Retrieved February 20, 2020.
  15. ↑ Gounaris, Anne D.; Turkenkopf, Iris; Buckwald, Sharon; Young, Anne (1971). "Pyruvate Decarboxylase I. Protein Dissociation into Subunits Under Conditions in which Thiamine Pyrophosphate is Released". Journal of Biological Chemistry. 246 (5): 1302–1309. doi: 10.1016/S0021-9258(19)76974-9 . PMID   5545074.
  16. ↑ National Institute of Communicative Disorders and Stroke (1979). NINCDS Index to Research Grants Subject Number Investigator & Contracts. National Institute of Health. pp. 253, 433.
  17. 1 2 Alexander, Garrett E.; Crutchner, Michael D (1990). "Functional architecture of basal ganglia circuits: neural substrates of parallel processing". Trends in Neurosciences. 13 (7): 266–271. doi:10.1016/0166-2236(90)90107-L. PMID   1695401. S2CID   3990601.
  18. ↑ Michigan Medicine (2020). "Movement Disorders Group Faculty". Movement Disorders Program. Retrieved February 20, 2020.
  19. ↑ "Venezuelan village key in search for Huntington's cure". BBC News. August 19, 2010. Retrieved February 20, 2020.
  20. ↑ Fish, Christi (March 21, 2011). "World-renowned neuroscientist Anne Young to speak on Huntington's disease March 24". UTSA Today. Retrieved February 20, 2020.
  21. 1 2 Harvard Catalyst (2020). "Anne Buckingham Young, Ph. D., M. D." Harvard Catalyst Profiles.
  22. ↑ ANA (2014). "ANA-NINDS Career Development Symposium". Americal Neurological Association. Retrieved February 20, 2020.
  23. ↑ Society for Neuroscience. "Summer 2005". Neuroscience Quarterly. Retrieved February 20, 2020.
  24. ↑ Society for Neuroscience. "Communicating Your Science to the Non-Expert". Neuronline.
  25. ↑ Young, Anne B.; Pert, Candace D.; Brown, David G.; Taylor, Kenneth M.; Snyder, Solomon H. (16 July 1971). "Nuclear Localization of Histamine in Neonatal Rat Brain". Science. 173 (3993): 247–249. doi:10.1126/science.173.3993.247. PMID   5104178. S2CID   38481674.
  26. ↑ Young, Anne B.; Oster-Granite, Mary Lou; Herndon, Robert M.; Snyder, Solomon H. (June 14, 1974). "Glutamic acid: Selective depletion by viral induced granule cell loss in hamster cerebellum". Brain Research. 73 (1): 1–13. doi:10.1016/0006-8993(74)91002-6. PMID   4152168 – via Elsevier.
  27. ↑ Maragos, William F.; Greenamyre, J. Timothy; Penney Jr., John B.; Young, Anne B. (February 1987). "Glutamate dysfunction in Alzheimer's disease: an hypothesis". Trends in Neurosciences. 10 (2): 65–68. doi:10.1016/0166-2236(87)90025-7. hdl: 2027.42/26817 . S2CID   53187290 – via Science Direct.
  28. ↑ McDonald, John W.; Johnston, Michael V. (1990). "Physiological and pathophysiological roles of excitatory amino acids during central nervous system development". Brain Research Reviews. 15 (1): 41–70. doi:10.1016/0165-0173(90)90011-C. hdl: 2027.42/28778 . PMID   2163714. S2CID   16878464.
  29. ↑ Reiner, Anton; Albin, Roger L.; Anderson, Keith D.; D'Amato, Constance J.; Penney, John B.; Young, Anne B. (August 1988). "Differential loss of striatal projection neurons in Huntington disease". Proceedings of the National Academy of Sciences. 85 (15): 5733–5737. Bibcode:1988PNAS...85.5733R. doi: 10.1073/pnas.85.15.5733 . PMC   281835 . PMID   2456581.
  30. ↑ Greenamyre, J. Timothy; Young, Anne B. (September 1989). "Excitatory amino acids and Alzheimer's disease". Neurobiology of Aging. 10 (5): 593–602. doi:10.1016/0197-4580(89)90143-7. hdl: 2027.42/27793 . PMID   2554168. S2CID   4045350 – via Elsevier.
  31. ↑ The Academic Family Tree (2020). "Neurotree: Anne B. Young". Neurotree. Retrieved February 20, 2020.
  32. ↑ U.S. News & World Report L.P. "About Dr. Anne B. Young MD". U.S. News & World Report: Health. Retrieved February 20, 2020.
  33. ↑ "Anne Buckingham Young". American Academy of Arts & Sciences. Retrieved 3 May 2019.
  34. ↑ Harvard University (2020). "JCSW Dean's Leadership Awards Previous Recipients" (PDF). The Joint Committee on the Status of Women. Retrieved February 20, 2020.
  35. ↑ Institute for Women's Health and Leadership (2020). "Past Marion Spencer Fay Award Honorees". Drexel University College of Medicine. Retrieved February 20, 2020.
  36. ↑ Hereditary Disease Foundation. "News from the Hereditary Disease Foundation" (PDF). Hereditary Disease Foundation Newsletter.
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