Started in 2010, The Minnesota Women Healthy Aging Project studies how brain changes with aging vary for different women and what might be the underlying causes of those differences. [1] Initiated by Apostolos Georgopoulos, a Regents Professor of Neuroscience at the University of Minnesota, [2] the premise for the project was inspired by a conversation with his wife, the endocrinologist Lily Georgopoulus, who had observed a small cohort of female patients who were thriving physically and mentally well into their 80s and 90s. [3] Georgopoulos is working with Lisa James, an associate professor of Neuroscience at the University of Minnesota [4] to construct a comprehensive, longitudinal database with information on cognitive abilities and genetic markers that can be used to understand the molecular biology of the aging brain. As of 2019, the study had enrolled over 100 women ranging in age from their 20s to 104 yrs old. Annual checkups are used to track the impact of genetic markers, brain images, diet, exercise and other lifestyle factors on cognitive changes in the women. The data has shown a link between a human leukocyte antigen and brain health [5] with the HLA-DRB1*13:02 allele correlating with less brain damage and with cognitive health over time. This observation provides a molecular mechanism to explain the widely published observation that infections by certain pathogens, such as herpes virus, contribute to loss of brain function and increased incidence of Alzheimer Disease. [6]
The fornix is a C-shaped bundle of nerve fibers in the brain that acts as the major output tract of the hippocampus. The fornix also carries some afferent fibers to the hippocampus from structures in the diencephalon and basal forebrain. The fornix is part of the limbic system. While its exact function and importance in the physiology of the brain are still not entirely clear, it has been demonstrated in humans that surgical transection—the cutting of the fornix along its body—can cause memory loss. There is some debate over what type of memory is affected by this damage, but it has been found to most closely correlate with recall memory rather than recognition memory. This means that damage to the fornix can cause difficulty in recalling long-term information such as details of past events, but it has little effect on the ability to recognize objects or familiar situations.
Aging of the brain is a process of transformation of the brain in older age, including changes all individuals experience and those of illness. Usually this refers to humans.
Imaging genetics refers to the use of anatomical or physiological imaging technologies as phenotypic assays to evaluate genetic variation. Scientists that first used the term imaging genetics were interested in how genes influence psychopathology and used functional neuroimaging to investigate genes that are expressed in the brain.
Cognitive reserve is the mind's and brain's resistance to damage of the brain. The mind's resilience is evaluated behaviorally, whereas the neuropathological damage is evaluated histologically, although damage may be estimated using blood-based markers and imaging methods. There are two models that can be used when exploring the concept of "reserve": brain reserve and cognitive reserve. These terms, albeit often used interchangeably in the literature, provide a useful way of discussing the models. Using a computer analogy, brain reserve can be seen as hardware and cognitive reserve as software. All these factors are currently believed to contribute to global reserve. Cognitive reserve is commonly used to refer to both brain and cognitive reserves in the literature.
Leukocyte immunoglobulin-like receptor subfamily B member 2 is a protein that in humans is encoded by the LILRB2 gene.
Protein KIBRA also known as kidney and brain expressed protein (KIBRA) or WW domain-containing protein 1 (WWC1) is a protein that in humans is encoded by the WWC1 gene.
In human neuroanatomy, brain asymmetry can refer to at least two quite distinct findings:
γ-L-Glutamyl-L-cysteine, also known as γ-glutamylcysteine (GGC), is a dipeptide found in animals, plants, fungi, some bacteria, and archaea. It has a relatively unusual γ-bond between the constituent amino acids, L-glutamic acid and L-cysteine and is a key intermediate in the γ-glutamyl cycle first described by Meister in the 1970s. It is the most immediate precursor to the antioxidant glutathione.
National Brain Research Centre is a research institute in Manesar, Gurgaon, India.It is an autonomous institute under the Department of Biotechnology, Ministry of Science and Technology, Government of India. The institute is dedicated to research in neuroscience and brain functions in health and diseases using multidisciplinary approaches. This is the first autonomous institute by DBT to be awarded by the Ministry of Education, Government of India, formerly known as the Ministry of Human Resource Development, in May 2002. NBRC was dedicated to the nation by the Honorable President of India Dr. A.P.J. Abdul Kalam in December 2003. The founder chairman of NBRC Society is Prof. Prakash Narain Tandon, whereas the founder director Prof. Vijayalakshmi Ravindranath was followed by Prof. Subrata Sinha and Prof. Neeraj Jain. The current director of NBRC is Prof. Krishanu Ray.
The Neurophysiological Biomarker Toolbox (NBT) is an open source MATLAB toolbox for the computation and integration of neurophysiological biomarkers. The NBT toolbox has so far been used in seven peer-reviewed research articles, and has a broad user base of more than 1000 users. The NBT toolbox provides unique features for analysis of resting-state EEG or MEG recordings. NBT offers a pipeline from data storage to statistics including artifact rejection, signal visualization, biomarker computation, statistical testing, and biomarker databasing. NBT allows for easy implementation of new biomarkers, and incorporates an online wiki that aims at facilitating collaboration among NBT users including extensive help and tutorials. The standardised way of data storage and analysis that NBT proposes allow different research projects to merge, compare, or share their data and biomarker algorithms.
A cerebral organoid, or brain organoid, describes an artificially grown, in vitro, miniature organ resembling the brain. Cerebral organoids are created by culturing pluripotent stem cells in a three-dimensional rotational bioreactor, and they develop over a course of months. The brain is an extremely complex system of heterogeneous tissues and consists of a diverse array of neurons. This complexity has made studying the brain and understanding how it works a difficult task in neuroscience, especially when it comes to neurodegenerative diseases. The purpose of creating an in vitro neurological model is to study these diseases in a more simple and variable space. This 3D model is free of many potential in vivo limitations. The varying physiology between human and other mammalian models limits the scope of study in neurological disorders. Cerebral organoids are synthesized tissues that contain several types of nerve cells and have anatomical features that recapitulate regions of the cortex observed in brains. Cerebral organoids are most similar to layers of neurons called the cortex and choroid plexus. In some cases, structures similar to the retina, meninges and hippocampus can form. Stem cells have the potential to grow into many different types of tissues, and their fate is dependent on many factors. Below is an image showing some of the chemical factors that can lead stem cells to differentiate into various neural tissues; a more in-depth table of generating specific organoid identity has been published since. Similar techniques are used on stem cells used to grow cerebral organoids.
Neuroenhancement or cognitive enhancement refers to the targeted enhancement and extension of cognitive and affective abilities based on an understanding of their underlying neurobiology in healthy persons who do not have any mental illness and outcomes in experimental research. As such, it can be thought of as an umbrella term that encompasses pharmacological and non-pharmacological methods of improving neurological functionality, especially interventions designed to improve human form or functioning beyond what is necessary to sustain or restore good health, as well as the overarching ethico-legal discourse that accompanies these aims and practices.
Neuroinflammation is inflammation of the nervous tissue. It may be initiated in response to a variety of cues, including infection, traumatic brain injury, toxic metabolites, or autoimmunity. In the central nervous system (CNS), including the brain and spinal cord, microglia are the resident innate immune cells that are activated in response to these cues. The CNS is typically an immunologically privileged site because peripheral immune cells are generally blocked by the blood–brain barrier (BBB), a specialized structure composed of astrocytes and endothelial cells. However, circulating peripheral immune cells may surpass a compromised BBB and encounter neurons and glial cells expressing major histocompatibility complex molecules, perpetuating the immune response. Although the response is initiated to protect the central nervous system from the infectious agent, the effect may be toxic and widespread inflammation as well as further migration of leukocytes through the blood–brain barrier may occur.
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.
Lisa James is an American clinical psychologist and a neuroscientist who works in the Departments of Neuroscience and Psychology at the University of Minnesota Medical School. She is also the Anita Kunin Professor of Healthy Brain Aging at the Brain Sciences Center at the Minneapolis VA Medical Center. In addition to research on post-traumatic stress disorders (PTSD) and resilience, she runs the longitudinal study for The Minnesota Women Healthy Aging Project.
The neurovascular unit (NVU) comprises the components of the brain that collectively regulate cerebral blood flow in order to deliver the requisite nutrients to activated neurons. The NVU addresses the brain's unique dilemma of having high energy demands yet low energy storage capacity. In order to function properly, the brain must receive substrates for energy metabolism–mainly glucose–in specific areas, quantities, and times. Neurons do not have the same ability as, for example, muscle cells, which can use up their energy reserves and refill them later; therefore, cerebral metabolism must be driven in the moment. The neurovascular unit facilitates this ad hoc delivery and, thus, ensures that neuronal activity can continue seamlessly.
Judith Ann Potashkin is an American professor at Rosalind Franklin University of Medicine and Science. She is best known for her research on diseases such as Parkinson's and Alzheimer's. She is an elected fellow of the American Association for the Advancement of Science.
Leukocyte immunoglobulin-like receptor subfamily A member 5 (LILR-A5) also known as CD85 antigen-like family member F (CD85f), immunoglobulin-like transcript 11 (ILT-11), and leukocyte immunoglobulin-like receptor 9 (LIR-9) is a protein that in humans is encoded by the LILRA5 gene. This gene is one of the leukocyte receptor genes that form a gene cluster on the chromosomal region 19q13.4. Four alternatively spliced transcript variants encoding distinct isoforms have been described.
Alzheimer's disease (AD) in the Hispanic/Latino population is becoming a topic of interest in AD research as Hispanics and Latinos are disproportionately affected by Alzheimer's Disease and underrepresented in clinical research. AD is a neurodegenerative disease, characterized by the presence of amyloid-beta plaques and neurofibrillary tangles, that causes memory loss and cognitive decline in its patients. However, pathology and symptoms have been shown to manifest differently in Hispanic/Latinos, as different neuroinflammatory markers are expressed and cognitive decline is more pronounced. Additionally, there is a large genetic component of AD, with mutations in the amyloid precursor protein (APP), Apolipoprotein E APOE), presenilin 1 (PSEN1), bridging Integrator 1 (BIN1), SORL1, and Clusterin (CLU) genes increasing one's risk to develop the condition. However, research has shown these high-risk genes have a different effect on Hispanics and Latinos then they do in other racial and ethnic groups. Additionally, this population experiences higher rates of comorbidities, that increase their risk of developing AD. Hispanics and Latinos also face socioeconomic and cultural factors, such as low income and a language barrier, that affect their ability to engage in clinical trials and receive proper care.
Alzheimer's disease (AD) in African Americans is becoming a rising topic of interest in AD care, support, and scientific research, as African Americans are disproportionately affected by AD. Recent research on AD has shown that there are clear disparities in the disease among racial groups, with higher prevalence and incidence in African Americans than the overall average. Pathologies for Alzheimer’s also seem to manifest differently in African Americans, including with neuroinflammation markers, cognitive decline, and biomarkers. Although there are genetic risk factors for Alzheimer’s, these account for few cases in all racial groups.