Behavioral neuroscience, also known as biological psychology, biopsychology, or psychobiology, is the application of the principles of biology to the study of physiological, genetic, and developmental mechanisms of behavior in humans and other animals.
The tau proteins are a group of six highly soluble protein isoforms produced by alternative splicing from the gene MAPT. They have roles primarily in maintaining the stability of microtubules in axons and are abundant in the neurons of the central nervous system (CNS), where the cerebral cortex has the highest abundance. They are less common elsewhere but are also expressed at very low levels in CNS astrocytes and oligodendrocytes.
The USC Leonard Davis School of Gerontology is one of the seventeen academic divisions of the University of Southern California in Los Angeles, focusing in undergraduate and graduate programs in gerontology,
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.
Pittsburgh compound B (PiB) is a radioactive analog of thioflavin T, which can be used in positron emission tomography scans to image beta-amyloid plaques in neuronal tissue. Due to this property, Pittsburgh compound B may be used in investigational studies of Alzheimer's disease.
Tauopathy belongs to a class of neurodegenerative diseases involving the aggregation of tau protein into neurofibrillary or gliofibrillary tangles in the human brain. Tangles are formed by hyperphosphorylation of the microtubule protein known as tau, causing the protein to dissociate from microtubules and form insoluble aggregates. The mechanism of tangle formation is not well understood, and whether tangles are a primary cause of Alzheimer's disease or play a peripheral role is unknown.
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, 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.
The biochemistry of Alzheimer's disease, the most common cause of dementia, is not yet very well understood. Alzheimer's disease (AD) has been identified as a proteopathy: a protein misfolding disease due to the accumulation of abnormally folded amyloid beta (Aβ) protein in the brain. Amyloid beta is a short peptide that is an abnormal proteolytic byproduct of the transmembrane protein amyloid-beta precursor protein (APP), whose function is unclear but thought to be involved in neuronal development. The presenilins are components of proteolytic complex involved in APP processing and degradation.
Bruce Sherman McEwen was an American neuroendocrinologist and head of the Harold and Margaret Milliken Hatch Laboratory of Neuroendocrinology at Rockefeller University. He was known for his work on the effects of environmental and psychological stress, having coined the term allostatic load.
George Perry is the former Dean of the College of Sciences, Semmes Distinguished University Chair in Neurobiology, Professor of Biology and Chemistry at the University of Texas at San Antonio. Perry is recognized in the field of Alzheimer's disease research particularly for his work on oxidative stress.
The prevention of dementia involves reducing the number of risk factors for the development of dementia, and is a global health priority needing a global response. Initiatives include the establishment of the International Research Network on Dementia Prevention (IRNDP) which aims to link researchers in this field globally, and the establishment of the Global Dementia Observatory a web-based data knowledge and exchange platform, which will collate and disseminate key dementia data from members states. Although there is no cure for dementia, it is well established that modifiable risk factors influence both the likelihood of developing dementia and the age at which it is developed. Dementia can be prevented by reducing the risk factors for vascular disease such as diabetes, high blood pressure, obesity, smoking, physical inactivity and depression. A study concluded that more than a third of dementia cases are theoretically preventable. Among older adults both an unfavorable lifestyle and high genetic risk are independently associated with higher dementia risk. A favorable lifestyle is associated with a lower dementia risk, regardless of genetic risk. In 2020, a study identified 12 modifiable lifestyle factors, and the early treatment of acquired hearing loss was estimated as the most significant of these factors, potentially preventing up to 9% of dementia cases.
Caleb Ellicott Finch is an American academic who is a professor at the USC Davis School of Gerontology. Finch's research focuses on aging in humans, with a specialization in cell biology and Alzheimer's disease.
Valter D. Longo is an Italian-American biogerontologist and cell biologist known for his studies on the role of fasting and nutrient response genes on cellular protection aging and diseases and for proposing that longevity is regulated by similar genes and mechanisms in many eukaryotes. He is currently a professor at the USC Davis School of Gerontology with a joint appointment in the department of Biological Sciences as well as serving as the director of the USC Longevity Institute.
The reproductive-cell cycle theory posits that the hormones that regulate reproduction act in an antagonistic pleiotrophic manner to control aging via cell cycle signaling; promoting growth and development early in life in order to achieve reproduction, but later in life, in a futile attempt to maintain reproduction, become dysregulated and drive senescence. Rather than seeing aging as a loss of functionality as we get older, this theory defines aging as any change in an organism over time, as evidenced by the fact that if all chemical reactions in the body were stopped, no change, and thus no aging, would occur. Since the most important change in an organism through time is the chemical reactions that result in a single cell developing into a multicellular organism, whatever controls these chemical reactions that regulate cell growth, development, and death, is believed to control aging. The theory argues that these cellular changes are directed by reproductive hormones of the hypothalamic-pituitary-gonadal axis. Receptors for reproductive hormones have been found to be present in all tissues of the body. Thus, HPG axis hormones normally promote growth and development of the organism early in life in order to achieve reproduction. Hormones levels then begin to change in men around age 30 and more abruptly in women when they reach menopause, around age 50. When the HPG axis becomes unbalanced, cellular growth and development is dysregulated, and cell death and dysfunction can occur, both of which can initiate senescence, the accumulated damage to cells, tissues, and organs that occurs with the passage of time and that is associated with functional loss during aging.
John P. Walsh, Ph.D. is an associate professor at the USC Davis School of Gerontology as well as a member of USC's Neuroscience Program. His main research interest is the physiology of basal ganglia-related brain disease.
The Institute of Gerontology (IOG) at Wayne State University conducts research on the behavioral and social aspects of aging. Located in Detroit, Michigan, the Institute has a strong focus on urban issues, especially disability, mobility and transportation, financial challenges, and disparities in health between ethnic groups. Faculty at the Institute are jointly appointed with a home department in a complementary discipline, such as economics, physical therapy or nursing. The Institute also maintains a Lifespan Cognitive Neuroscience of Aging laboratory currently profiling brain changes in normal aging through traditional testing and magnetic resonance imaging (MRI) of participants brain structure and function.
Neuroangiogenesis is the coordinated growth of nerves and blood vessels. The nervous and blood vessel systems share guidance cues and cell-surface receptors allowing for this synchronised growth. The term neuroangiogenesis only came into use in 2002 and the process was previously known as neurovascular patterning. The combination of neurogenesis and angiogenesis is an essential part of embryonic development and early life. It is thought to have a role in pathologies such as endometriosis, brain tumors, and Alzheimer's disease.
RAD140 is an investigational selective androgen receptor modulator (SARM) that is developed by Radius Health, Inc. for use in androgen replacement therapy. It was licensed to Ellipses Pharmaceuticals in 2020. Some of the potential benefits under investigation are for the treatment of conditions such as muscle wasting and bone loss.
Giulio Maria Pasinetti is the Program Director of the Center on Molecular Integrative Neuroresilience and is the Saunders Family Chair in Neurology at the Icahn School of Medicine at Mount Sinai (ISMMS) in New York City. Pasinetti is a Professor of Neurology, Psychiatry, Neuroscience, and Geriatrics and Palliative Medicine at ISMMS.
Donald L. Price is an American neuropathologist and professor at the Johns Hopkins School of Medicine born in Stamford, Connecticut. His research aims to understand the molecular basis of neurodegenerative diseases, particularly Alzheimer’s disease. Price has received a number of awards for his work and served as the President of both the American Association of Neuropathologists and the Society for Neuroscience.
