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Degenerative Diseases of the Nervous System
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
James A. Mastrianni, Elizabeth A. Harris
NFTs (Figures 16.5–16.8) are intracellular lesions principally composed of aggregations of a hyperphosphorylated form of the cytoskeletal-associated microtubular protein, tau. The aggregated neurofibrils are visualized as paired helical filaments on electron microscopy. They are present, together with plaques, in the projection neurons of the limbic and association areas of the cerebral cortex, particularly the parietal cortex and hippocampus, especially the CA1 zone and the entorhinal cortex, subiculum, and transitional cortex of the hippocampus.
The Nervous System and Its Disorders
Published in Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss, Understanding Medical Terms, 2020
Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss
Some axons are surrounded by a myelin sheath (neurilemma or neurolemma) consisting of the lipid substance myelin. The myelin sheath is discontinuous approximately every millimeter at the neurofibril nodes, also called the nodes of Ranvier. The myelin serves as an electrical insulator, forcing the impulse to jump from one node to another, which functions to increase the speed of conduction in a myelinated nerve and decrease the energy required for transmission. Further, the larger a nerve is, the more quickly it can conduct impulses. Because of their speed of conduction, large myelinated nerves are the primary conductors of impulses to skeletal muscles, allowing the rapid responses
Role of Herbs and Their Delivery Through Nanofibers in Pharmacotherapy of Depression
Published in Anne George, Snigdha S. Babu, M. P. Ajithkumar, Sabu Thomas, Holistic Healthcare. Volume 2: Possibilities and Challenges, 2019
Ginpreet Kaur, Mihir Invally, Hiral Mistry, Parnika Dicholkar, Sukhwinder Bhullar
It is a type of dementia which attacks 30 million people throughout the world.2 Symptoms of Alzheimer’s include loss of memory, judgment, and thinking which prevent the patient from performing daily activities. It is characterized by amyloid plaques, neurofibrillary tangles, and loss of cholinergic neurons. There is synapse loss due to the aggregation of amyloid-beta (α,β) into senile plaques and “tau” protein into neurofibril-lary tangles which leads to neurodegeneration and causes Alzheimer’s.5
Bio-chemical markers of chronic, non-infectious disease in the human tear film
Published in Clinical and Experimental Optometry, 2022
Sultan Alotaibi, Maria Markoulli, Jerome Ozkan, Eric Papas
Alzheimer’s disease is the most common form of dementia, influencing the daily life of 30 million people across the world with rising prevalence.96 The underlying causes of Alzheimer’s disease are unknown and under investigation but pathogenesis is linked to the accumulation of neurofibril tangles inside the neurons and the aggregation of amyloid plaques in the interstices.97 Deposition of Tau proteins, which are microtubule associated proteins involved in neuronal function,98 creates neurofibrillary tangles, while amyloid plaques are formed by beta-amyloid peptides.99 In normal brain tissue, beta-amyloid is broken down and eliminated, but in Alzheimer’s disease, removal is incomplete and the resulting plaques are characteristic of the condition.100 In addition, the pre-synaptic protein synuclein (as discussed above) may have a role in the pathogenesis of the disease.101
The emerging role of the sigma-1 receptor in autophagy: hand-in-hand targets for the treatment of Alzheimer’s
Published in Expert Opinion on Therapeutic Targets, 2021
Mani Iyer Prasanth, Dicson Sheeja Malar, Tewin Tencomnao, James Michael Brimson
AD is a neurodegenerative disease that is characterized by amyloid β (Aβ) plaques in the brain, excessive tau-protein phosphorylation, and neurofibril tangles, which lead to a decline in cognitive ability of the individual. AD is responsible for 60–70% of dementia cases, resulting in approximately 44 million cases worldwide. As the world’s population increases, there is expected to be up to 135 million cases by 2050, which will account for over half those aged over 65 years. Currently, AD costs the world over 600 billion US dollars, which is equivalent to 1% of the world's GDP [14]. The risk of developing AD depends largely on genetics [15], with polymorphisms in genes, such as the amyloid precursor protein (APP), presenilin-1, and presenilin-2 thought to be largely responsible for familial (early onset) AD, whereas the presence of the allele ε4 of the apolipoprotein E (APOE) increases the risk for sporadic (late onset) AD [16]. Polymorphisms in these genes combined with acquired risk factors such as increasing age [17], along with long-term lack of quality sleep [18,19], poor diet [20] leading to high cholesterol, hypertension, and type-2 diabetes led to the development of AD.
Polysaccharide of Taxus chinensis var. mairei Cheng et L.K.Fu attenuates neurotoxicity and cognitive dysfunction in mice with Alzheimer’s disease
Published in Pharmaceutical Biology, 2020
Senwei Zhang, Lulu Li, Jinting Hu, Ping Ma, Huimin Zhu
Intertwining of neurofibrils, loss of neurons and senile plaque formation are important pathological features in the brain of AD patients (Chandra 2017). Aβ is considered to be the most important component of senile plaque (Chandra 2017). Excessive Aβ deposits outside the cortex and hippocampal neurons, forming plaque tangles that lead to abnormal synaptic function, loss of nerve cells and inflammation, eventually leading to neurological structural and functional disorders and the formation of dementia (Nasica-Labouze et al. 2015). Besides, abnormal Aβ is able to induce apoptosis and neurotoxicity (Lee et al. 2013; Porcellotti et al. 2015). Interestingly, Aβ may affect cell apoptosis by regulating the activity of caspase-3, which plays an irreplaceable role in the process of apoptosis (Chang et al. 2016). Our results indicated that PTM treatment could reduce Aβ expression and apoptosis-related protein cleaved caspase-3 and Bax/Bcl-2 ratio in AD-like mice.