Eva Braak | |
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| Born | November 26, 1939 |
| Died | July 25, 2000 |
| Education | Georg August University, Vogt Institute for Brain Research - University of Dusseldorf, University of Kiel |
| Occupation(s) | Anatomist, professor |
Eva Braak (1939-2000) was a German anatomist, mostly known for the Braak and Braak Alzheimer disease stages. [1] She was professor at the Institute of Clinical Neuroanatomy, Johann Wolfgang Goethe-University, Frankfurt am Main.
Eva Braak and her husband, Heiko Braak, were in charge of a group investigating new techniques in the study of degenerative diseases of the brain [2] In the 1970s, Braak and her husband implemented and perfected the than-new silver-iodate histological technique to study relatively thick sections of whole brains, up to 150 microns. [3] Using those methods, they contributed extensively to the neuropathology of Alzheimer's and Parkinson's diseases. In 1987, Braak and her husband were the first to describe the pathological changes of argyrophilic grain disease, an unknown tauopathy which was previously marked as senile dementia. [4] A few years later, in 1991, they introduced a classification of Alzheimer's disease into six distinct pathoanatomical stages, now commonly known as Braak and Braak stages, based on the topographical distribution pattern of neurofibrillary changes from circumscribed parts of the limbic system to the higher neocortical association fields. [1] Eva Braak was the first female scientist to receive an Award for Life-time Achievements in Alzheimer's Disease Research, granted during the Sixth International Conference on Alzheimer's Disease and related Disorders, in 1998. [5]
She died of ovarian cancer on 25 August 2000 in Frankfurt am Main. [6]
Alois Alzheimer was a German psychiatrist and neuropathologist and a colleague of Emil Kraepelin. Alzheimer is credited with identifying the first published case of "presenile dementia", which Kraepelin would later identify as Alzheimer's disease.
Lewy bodies are the inclusion bodies – abnormal aggregations of protein – that develop inside nerve cells affected by Parkinson's disease (PD), the Lewy body dementias, and some other disorders. They are also seen in cases of multiple system atrophy, particularly the parkinsonian variant (MSA-P).
Progressive supranuclear palsy (PSP) is a late-onset neurodegenerative disease involving the gradual deterioration and death of specific volumes of the brain. The condition leads to symptoms including loss of balance, slowing of movement, difficulty moving the eyes, and cognitive impairment. PSP may be mistaken for other types of neurodegeneration such as Parkinson's disease, frontotemporal dementia and Alzheimer's disease. The cause of the condition is uncertain, but involves the accumulation of tau protein within the brain. Medications such as levodopa and amantadine may be useful in some cases.
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.
Amyloid plaques are extracellular deposits of the amyloid beta (Aβ) protein mainly in the grey matter of the brain. Degenerative neuronal elements and an abundance of microglia and astrocytes can be associated with amyloid plaques. Some plaques occur in the brain as a result of aging, but large numbers of plaques and neurofibrillary tangles are characteristic features of Alzheimer's disease. The plaques are highly variable in shape and size; in tissue sections immunostained for Aβ, they comprise a log-normal size distribution curve, with an average plaque area of 400-450 square micrometers (µm²). The smallest plaques, which often consist of diffuse deposits of Aβ, are particularly numerous. Plaques form when Aβ misfolds and aggregates into oligomers and longer polymers, the latter of which are characteristic of amyloid.
Frontotemporal lobar degeneration (FTLD) is a pathological process that occurs in frontotemporal dementia. It is characterized by atrophy in the frontal lobe and temporal lobe of the brain, with sparing of the parietal and occipital lobes.
Neurofibrillary tangles (NFTs) are intracellular aggregates of hyperphosphorylated tau protein that are most commonly known as a primary biomarker of Alzheimer's disease. Their presence is also found in numerous other diseases known as tauopathies. Little is known about their exact relationship to the different pathologies.
Tauopathies are neurodegenerative diseases involving the aggregation of abnormal tau protein. Tangles are formed by hyperphosphorylation of the microtubule protein known as tau, causing the protein to dissociate from microtubules and form insoluble aggregate. Various neuropathologic phenotypes are identified based on the specific engagement of anatomical regions, cell types, and the presence of unique isoforms of tau within pathological deposits. The designation 'primary tauopathy' is assigned to disorders where the predominant feature is the deposition of tau protein. Alternatively, diseases exhibiting tau pathologies attributed to different and varied underlying causes are termed 'secondary tauopathies. Some neuropathologic phenotypes involving tau protein is Alzheimer’s disease, Pick disease, Progressive supranuclear palsy and corticobasal degeneration.
β-Methylamino-L-alanine, or BMAA, is a non-proteinogenic amino acid produced by cyanobacteria. BMAA is a neurotoxin. Its potential role in various neurodegenerative disorders is the subject of scientific research.
Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease linked to repeated trauma to the head. The encephalopathy symptoms can include behavioral problems, mood problems, and problems with thinking. The disease often gets worse over time and can result in dementia.
Transmembrane protein 106B is a protein that is encoded by the TMEM106B gene. It is found primarily within neurons and oligodendrocytes in the central nervous system with its subcellular location being in lysosomal membranes. TMEM106B helps facilitate important functions for maintaining a healthy lysosome, and therefore certain mutations and polymorphisms can lead to issues with proper lysosomal function. Lysosomes are in charge of clearing out mis-folded proteins and other debris, and thus, play an important role in neurodegenerative diseases that are driven by the accumulation of various mis-folded proteins and aggregates. Due to its impact on lysosomal function, TMEM106B has been investigated and found to be associated to multiple neurodegenerative diseases.
Heiko Braak is a German anatomist. Braak was born in Kiel, Schleswig-Holstein, and studied medicine at the universities of Hamburg, Berlin, and Kiel. He was Professor at the Institute of Clinical Neuroanatomy, Johann Wolfgang Goethe-University, Frankfurt am Main. Currently he is based at the 'Clinical Neuroanatomy Section, Department of Neurology, Center for Biomedical Research, University of Ulm, Germany.
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 typical life expectancy following diagnosis is three to nine years.
The applause sign is a behavioural indicator, relevant to neurodegenerative conditions, characterised by a patient’s inability to execute the same number of hand claps as demonstrated by an examiner.
Braak staging refers to two methods used to classify the degree of pathology in Parkinson's disease and Alzheimer's disease. These methods are used both in research and for the clinical diagnosis of these diseases and are obtained by performing an autopsy of the brain.
Florbetaben, a fluorine-18 (18F)-labeled stilbene derivative, trade name NeuraCeq, is a diagnostic radiotracer developed for routine clinical application to visualize β-amyloid plaques in the brain. It is indicated for Positron Emission Tomography (PET) imaging of β-amyloid neuritic plaque density in the brains of adult patients with cognitive impairment who are being evaluated for Alzheimer's disease (AD) and other causes of cognitive impairment. β-amyloid is a key neuropathological hallmark of AD, so markers of β-amyloid plaque accumulation in the brain are useful in distinguishing AD from other causes of dementia. The tracer successfully completed a global multicenter phase 0–III development program and obtained approval in Europe, US and South Korea in 2014.
Synucleinopathies are neurodegenerative diseases characterised by the abnormal accumulation of aggregates of alpha-synuclein protein in neurons, nerve fibres or glial cells. There are three main types of synucleinopathy: Parkinson's disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA). Other rare disorders, such as various neuroaxonal dystrophies, also have α-synuclein pathologies. Additionally, autopsy studies have shown that around 6% of sporadic Alzheimer's Disease exhibit α-synuclein positive Lewy pathology, and are sub-classed as Alzheimer's Disease with Amygdalar Restricted Lewy Bodies (AD/ALB).
Primary age-related tauopathy (PART) is a neuropathological designation introduced in 2014 to describe the neurofibrillary tangles (NFT) that are commonly observed in the brains of normally aged and cognitively impaired individuals that can occur independently of the amyloid plaques of Alzheimer's disease (AD). The term and diagnostic criteria for PART were developed by a large group of neuropathologists, spearheaded by Drs. John F. Crary and Peter T. Nelson. Despite some controversy, the term PART has been widely adopted, with the consensus criteria cited over 1130 times as of April 2023 according to Google Scholar.
LATE is a term that describes a prevalent condition with impaired memory and thinking in advanced age, often culminating in the dementia clinical syndrome. In other words, the symptoms of LATE are similar to those of Alzheimer's disease.
Granulovacuolar degeneration refers to the occurrence within neurons of abnormal, fluid-filled bubbles (vacuoles) containing a dense proteinaceous granule. Granulovacuoles occur most commonly in pyramidal neurons of the hippocampus. They are present in small numbers in non-demented elderly people, but increase in frequency in Alzheimer's disease and other tauopathies. In Alzheimer's disease, granulovacuoles proliferate stage-wise in different brain areas, and their prevalence is correlated with the degree of tauopathy, Abeta plaque pathology, and cerebral amyloid angiopathy. Immunohistochemical analyses have found that the inner granule includes several proteins, including tubulin tau protein, TDP-43 and others. Although granulovacuoles and their functional significance are still poorly understood, they have been compared to autophagic vacuoles
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