Synonyms for ftld or Related words with ftld

nondemented              bvftd              dlbd              fxtas              neuropathologically              bfie              mtle              bfnc              ftd              neuropathology              cadasil              fsgs              lafora              lissencephaly              ancg              scjd              taupathies              llmd              amyloidopathies              mpgnii              progeria              cidp              narp              neuropathologic              neuropathological              epilepsies              drpla              tauopathy              endophenotype              edmd              kindreds              sclerosteosis              laminopathies              amci              endophenotypes              probands              ataxiadystonia              lincl              proteinopathy              nonsyndromic              rolandic              schizophrenic              progeroid              fcjd              arvc              dravet              arvcf              schizophrenics              hibm              neuronopathy             

Examples of "ftld"
There have been numerous advances in descriptions of genetic causes of FTLD, and the related disease amyotrophic lateral sclerosis.
Of all the FTLD syndromes SD is least likely to run in families and is usually sporadic.
SD is one of the three canonical clinical syndromes associated with frontotemporal lobar degeneration (FTLD). SD is a clinically defined syndrome, but is associated with predominantly temporal lobe atrophy (left greater than right) and hence is sometimes called temporal variant FTLD (tvFTLD).
United States Senator Pete Domenici (R-NM) is a known sufferer of FTLD, and the illness is the main reason behind his October 4, 2007 announcement of retirement at the end of his term. American film director, producer, and screenwriter Curtis Hanson died as a result of FTLD on September 20, 2016.
Common proteinopathies that are found in FTLD include the accumulation of Tau proteins and TARDBPs. Mutations in the C9orf72 gene have been established as a major genetic contribution of FTLD, although defects in the GRN and MAPT genes are also associated with it.
Frontotemporal lobar degeneration (FTLD) is a neurodegenerative disease that attacks the brain selectively in the frontal lobe, temporal lobe and amygdala. Patients suffering from FTLD offer information on the biological complexity involved in generating self-conscious emotions. With the use of a startle experiment (where patients and control participants are exposed to an unexpected and loud sound) it has been shown that sufferers of FTLD show and experience the basic negative emotions expected to be attached to the startling sounds. However they show significantly less signs of experiencing self-conscious emotions compared to control groups. This is due to an inhibition of embarrassment caused by the damaged brain (Sturm & Rosen, 2006).
There are 3 main histological subtypes found at post-mortem: FTLD-tau, FTLD-TDP, and FTLD-FUS. Dementia lacking distinctive histology (DLDH) is a rare and controversial entity. New analyses has allowed many cases previously described as DLDH to be reclassified into one of the positively defined subgroups. In rare cases, patients with clinical FTD were found to have changes consistent with Alzheimer's disease on autopsy. The most severe brain atrophy appears to be associated with Pick's disease, corticobasal degeneration, and TDP pathology associated with behavioral-variant FTD.
Mutations in all of the above genes cause a very small fraction of the FTLD spectrum. Most of the cases are sporadic (no known genetic cause).
FTLD is the pathological term for the clinical syndrome of frontotemporal dementia (FTD). FTD differs from the more common Alzheimer's dementia in that memory is relatively well preserved, instead the disease presents with a more temporal-lobe phenotype. Behavioural variant frontotemporal dementia (bvFTD), progressive non-fluent aphasia (PNFA) and semantic dementia (SD) are the three best-characterised clinical presentations. FUS positive FTLD tends to present clinically as a bvFTD but the correlation between underlying pathology and clinical presentation is not perfect.
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.
Frontotemporal lobar degeneration (FTLD) is a common form of dementia due to the degeneration of the frontal and temporal lobes. Studies have found significant decreases in the essential needs for proper functioning in these lobes. The autobiographical domain in memory is largely affected by this disease. In one study, FTLD patients were interviewed and asked to describe a significant event from five different periods of their lives. Using the interview and different methods of imaging, the experimenters hoped to find links between patterns of brain volume loss and performance in the interview.
A hyper-phosphorylated, ubiquitinated and cleaved form of TDP-43—known as pathologic TDP43—is the major disease protein in ubiquitin-positive, tau-, and alpha-synuclein-negative frontotemporal dementia (FTLD-TDP, previously referred to as FTLD-U) and in Amyotrophic lateral sclerosis (ALS). Elevated levels of the TDP-43 protein have also been identified in individuals diagnosed with chronic traumatic encephalopathy, a condition that often mimics ALS and that has been associated with athletes who have experienced multiple concussions and other types of head injury. Abnormalities of TDP-43 also occur in an important subset of Alzheimer's disease patients, correlating with clinical and neuropathologic features indexes.
The ability to show basic emotions while lacking the ability to perform the more complex self-conscious emotions demonstrates that self-conscious emotions are biologically harder to perform than average emotions. It should also be noted that FTLD patients tend to struggle in social situations (Sturm & Rosen, 2006). This is again linked with their inability to perform self-conscious emotions adequately.
Through image processing, patterns of significant reduced parenchymal volumes that encompass the frontal and temporal lobes were found. Through comparison to a control group of patients it was found that parenchymal volumes increased during episodic recall, and decreased during semantic recall. The experimenters discussed that lifespan autobiographical episodic recall was largely damaged in FTLD patients and semantic autobiographical memory seemed to be spared.
Proteintech Group’s antibodies have been successful in several research areas. For example, the antibody against TAR DNA-binding protein 43 has featured in many publications investigating its role in many neuropathologies including: ALS, FTLD, Alzheimer's disease. Parkinson's disease Lewy body disease Huntington's Disease and Machado-Joseph disease Proteintech was also the first company to provide a commercially available FKBPL antibody. This has been most notably used in a study to determine the response of breast cancer patients to the drug Tamoxifen.
For >15 years, Dr. Trojanowski has conducted research on AD, PD, motor neuron disease, dementia with Lewy bodies (DLB), frontotemporal lobar degeneration (FTLD) and other aging related nervous system disorders. Most of his >500 publications focus on the pathobiology of neurodegenerative disorders, especially the role of abnormal protein aggregates (misfolded proteins) in these diseases. The major goal of his research now is to translate advances into understanding mechanisms of aging related neurodegenerative diseases into meaningful interventions to treat or prevent these disorders.
Subsequently, FUS has also emerged as a significant disease protein in a subgroup of frontotemporal lobar dementias (FTLDs), previously characterized by immunoreactivity of the neuronal inclusions for ubiquitin, but not for TDP-43 or tau with a proportion of the inclusions also containing a-internexin in a further subgroup known as neuronal intermediate filament inclusion disease (NIFID). The disease entities which are now considered subtypes of FTLD-FUS are atypical frontotemporal lobar degeneration with ubiquitinated inclusions (aFTLD-U), NIFID (otherwise known as neurofilament inclusion body disease) and basophilic inclusion body disease (BIBD), which together with ALS-FUS comprise the FUS-opathies.
Bioinformatic screens have predicted that over 250 human proteins contain prion-like domains (PrLD). These domains are hypothesized to have the same transmissible, amyloidogenic properties of PrP and known fungal proteins. As in yeast, proteins involved in gene expression and RNA binding seem to be particularly enriched in PrLD's, compared to other classes of protein. In particular, 29 of the known 210 proteins with an RNA recognition motif also have a putative prion domain. Meanwhile, several of these RNA-binding proteins have been independently identified as pathogenic in cases of ALS, FTLD-U, Alzheimer's disease, and Huntington's disease.
In later stages of FTLD, the clinical phenotypes may overlap. FTD patients tend to struggle with binge eating and compulsive behaviors. These binge eating habits are often associated with abnormal eating behavior including overeating, stuffing oneself with food, changes in food preferences (cravings for more sweets, carbohydrates), eating inedible objects and snatching food from others. Recent findings have indicated that the neural structures responsible for eating changes in FTD include atrophy in the right ventral insula, striatum and orbitofrontal cortex on structural MRI voxel-based morphometry (right hemisphere).
Primary progressive aphasia (PPA) is a type of neurological syndrome in which language capabilities slowly and progressively become impaired. Although it was first described as solely impairment of language capabilities while other mental functions remain intact, it is now recognized that many, if not most of those afflicted suffer impairment of memory, short term memory formation and loss of executive functions. It was first described as a distinct syndrome by M.-Marsel Mesulam in 1982. Primary progressive aphasias have a clinical and pathological overlap with the frontotemporal lobar degeneration (FTLD) spectrum of disorders and Alzheimer's disease.