Martin Rossor | |
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| Professor of Neurology, University College London | |
| In office 1998–2015 | |
| Personal details | |
| Born | 24 April 1950 |
| Occupation | Neurologist |
Martin Neil Rossor (born 24 April 1950) is a British clinical neurologist with a specialty interest in degenerative dementias and familial disease.
He is professor emeritus and principal research associate at the UCL Queen Square Institute of Neurology, honorary consultant neurologist at the National Hospital for Neurology and Neurosurgery, and was the national director for Dementia Research for the National Institute for Health Research (NIHR) in the UK.
He was the editor of the Journal of Neurology, Neurosurgery, and Psychiatry , president of the Association of British Neurologists, director of the NIHR Clinical Research Network for Dementia and Neurodegenerative Diseases, and director of the NIHR Queen Square Dementia Biomedical Research Unit. [1] [2]
His collaborative work in identifying and characterising a large collection of familial cases of Alzheimer’s disease contributed to the discovery of mutations in the amyloid precursor protein gene. [3] [4]
His recent research focuses on general cognitive impairment in systemic disease and multimorbidity including development of the Cognitive Footprint concept, which he co-authored in 2015. [5]
Rosser attended Jesus College, Cambridge (1968-1971); and King's College, Hospital Medical School (1971-1974).
He holds a Bachelor of Medicine/ Bachelor of Surgery (1974); Master of Arts (1975); is a Member of the Royal College of Physicians (1976); Doctor of Medicine (1986); and Fellow of the Royal College of Physicians (1990). [6]
In 2022, he was elected a member of the Academia Europaea. [7]
Rossor has authored nearly 900 publications. He has been on the Highly Cited Researcher list from Clarivate since 2018. [8]
Amyloid beta denotes peptides of 36–43 amino acids that are the main component of the amyloid plaques found in the brains of people with Alzheimer's disease. The peptides derive from the amyloid-beta precursor protein (APP), which is cleaved by beta secretase and gamma secretase to yield Aβ in a cholesterol-dependent process and substrate presentation. Both neurons and oligodendrocytes produce and release Aβ in the brain, contributing to formation of amyloid plaques. Aβ molecules can aggregate to form flexible soluble oligomers which may exist in several forms. It is now believed that certain misfolded oligomers can induce other Aβ molecules to also take the misfolded oligomeric form, leading to a chain reaction akin to a prion infection. The oligomers are toxic to nerve cells. The other protein implicated in Alzheimer's disease, tau protein, also forms such prion-like misfolded oligomers, and there is some evidence that misfolded Aβ can induce tau to misfold.
Amyloid-beta precursor protein (APP) is an integral membrane protein expressed in many tissues and concentrated in the synapses of neurons. It functions as a cell surface receptor and has been implicated as a regulator of synapse formation, neural plasticity, antimicrobial activity, and iron export. It is coded for by the gene APP and regulated by substrate presentation. APP is best known as the precursor molecule whose proteolysis generates amyloid beta (Aβ), a polypeptide containing 37 to 49 amino acid residues, whose amyloid fibrillar form is the primary component of amyloid plaques found in the brains of Alzheimer's disease patients.
A neurodegenerative disease is caused by the progressive loss of neurons, in the process known as neurodegeneration. Neuronal damage may also ultimately result in their 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.
Sir John Anthony Hardy is a human geneticist and molecular biologist at the Reta Lila Weston Institute of Neurological Studies at University College London with research interests in neurological diseases.
The Roskamp Institute, was co-founded by Robert and Diane Roskamp, and Fiona Crawford and Michael Mullan in Sarasota, Florida in 2003. It is a nonprofit biomedical research facility specializing neurological research including Alzheimer's disease, traumatic brain injury, Gulf War syndrome, and posttraumatic stress disorder. It also operates an onsite neurology clinic. The institute is focused on finding the causes and treatments for neuropsychiatric and neurodegenerative diseases.
Bart De Strooper is a Belgian molecular biologist and professor at Vlaams Instituut voor Biotechnologie and KU Leuven and the UK Dementia Research Institute and University College London, UK. De Strooper's research seeks to translate genetic data into the identification and treatment of neurodegenerative diseases and treatments. interest are the secretases, proteases which cleave the amyloid precursor protein (APP), resulting in amyloid peptides.
Michael Mullan is an English-American researcher in Alzheimer's disease and related neurodegenerative disorders. Mullan was a co-discoverer of genetic causes of Alzheimer's disease. Subsequently, he was a co-inventor on the original patents that covered three mutations in the amyloid precursor protein (APP) gene, a gene which is linked to familial Alzheimer's disease. He also co-authored articles in Nature and Nature Genetics, describing these three genetic errors; he was the senior author on two of those articles. Dr. Mullan co-discovered a specific genetic mutation, which became known as "the Swedish Mutation," because it was originally identified in DNA samples from two Swedish families whose members often developed early-onset Alzheimer's disease. These human genetic mutations were integrated into mouse DNA to create strains of mice that are being used worldwide to develop new drug treatments for Alzheimer's disease.
Alzheimer's disease (AD) is a neurodegenerative disease that usually starts slowly and progressively worsens, and is the cause of 60–70% of cases of dementia. The most common early symptom is difficulty in remembering recent events. As the disease advances, symptoms can include problems with language, disorientation, mood swings, loss of motivation, self-neglect, and behavioral issues. As a person's condition declines, they often withdraw from family and society. Gradually, bodily functions are lost, ultimately leading to death. Although the speed of progression can vary, the average life expectancy following diagnosis is three to twelve years.
Early-onset Alzheimer's disease (EOAD), also called younger-onset Alzheimer's disease (YOAD), is Alzheimer's disease diagnosed before the age of 65. It is an uncommon form of Alzheimer's, accounting for only 5–10% of all Alzheimer's cases. About 60% have a positive family history of Alzheimer's and 13% of them are inherited in an autosomal dominant manner. Most cases of early-onset Alzheimer's share the same traits as the "late-onset" form and are not caused by known genetic mutations. Little is understood about how it starts.
Peter Henry St George-Hyslop is a British and Canadian medical scientist, neurologist and molecular geneticist who is known for his research into neurodegenerative diseases. St George-Hyslop is one of the most cited authors in the field of Alzheimer's disease research. He has identified a number of key genes that are responsible for nerve cell degeneration and early-onset forms of Alzheimer's disease. These include the discovery of the presenilins, Nicastrin, TREM2, Apolipoprotein E and SORL1 genes. Presenilin mutations are the most common cause of familial Alzheimer's disease. St George-Hyslop also co-led the discovery of the gene for the amyloid precursor protein.
The Swedish mutation, or familial Alzheimer's disease genetic mutation, is one of the most well known genetic variations that causes early-onset familial Alzheimer's disease.
Philip Scheltens is a Dutch professor of neurology and founder of the Alzheimer Centre, Amsterdam University Medical Centers, location VUmc in Amsterdam.
Colin Louis MastersMD is an Australian neuropathologist who researches Alzheimer's disease and other neurodegenerative disorders. He is laureate professor of pathology at the University of Melbourne.
Alison Mary Goate is the Jean C. and James W. Crystal Professor and Chair of the Department of Genetics and Genomic Sciences and Director of the Loeb Center for Alzheimer's Disease at Icahn School of Medicine at Mount Sinai, New York City. She was previously professor of genetics in psychiatry, professor of genetics, and professor of neurology at Washington University School of Medicine.
Mary M. Reilly FRCP is an Irish neurologist who works at National Hospital for Neurology and Neurosurgery. She studies peripheral neuropathy. She is the President of the Association of British Neurologists.
Dennis J. Selkoe is an American physician (neurologist) known for his research into the molecular basis of Alzheimer's disease. In 1985 he became Co-Director of the Center for Neurological Diseases and from 1990, Vincent and Stella Coates Professor of Neurological Diseases at Harvard Medical School. He is also a Fellow of the AAAS and a member of the National Academy of Medicine.
Familial Danish dementia is an extremely rare, neurodegenerative disease characterized by progressive cataracts, loss of hearing, cerebellar ataxia, paranoid psychosis, and dementia. Neuropathological hallmarks include extensive atrophy of all areas of the brain, chronic diffuse encephalopathy, and the presence of exceedingly thin and nearly totally demyelinated cranial nerves.
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.
Carol Joyce Jennings was a British campaigner and advocate for research into Alzheimer's disease. She served as an honorary Vice-President of the Alzheimer's Society until her death in 2024. Through her activism in the 1980s, Jennings brought her family to the attention of researchers studying the disease, which subsequently led to the discovery of the London Mutation. This mutation, found on the Amyloid Precursor Protein (APP) gene located on chromosome 21, marked a significant breakthrough in understanding the genetic basis of Alzheimer's disease and provided evidence for the development of the 'amyloid hypothesis', which attempts to explain the underlying causes of Alzheimer's disease.
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