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Browse result for Dementia with Lewy bodies

※ introduction

    Dementia with Lewy bodies (DLB) is a type of dementia characterized by changes in sleep, behavior, cognition, movement, and regulation of automatic bodily functions. Memory loss is not always an early symptom. The disease worsens over time and is usually diagnosed when cognitive impairment interferes with normal daily functioning. Together with Parkinson's disease dementia, DLB is one of the two Lewy body dementias. It is a common form of dementia, but the prevalence is not known accurately and many diagnoses are missed. The disease was first described on autopsy by Kenji Kosaka in 1976, and he named the condition several years later. REM sleep behavior disorder (RBD)¡ªin which people lose the muscle paralysis (atonia) that normally occurs during REM sleep and act out their dreams¡ªis a core feature. RBD may appear years or decades before other symptoms. Other core features are visual hallucinations, marked fluctuations in attention or alertness, and parkinsonism (slowness of movement, trouble walking, or rigidity). A presumptive diagnosis can be made if several disease features or biomarkers are present; the diagnostic workup may include blood tests, neuropsychological tests, imaging, and sleep studies. A definitive diagnosis usually requires an autopsy. Most people with DLB do not have affected family members, although occasionally DLB runs in a family. The exact cause is unknown but involves formation of abnormal clumps of protein in neurons throughout the brain. Manifesting as Lewy bodies (discovered in 1912 by Frederic Lewy) and Lewy neurites, these clumps affect both the central and the autonomic nervous systems. Heart function and every level of gastrointestinal function¡ªfrom chewing to defecation¡ªcan be affected, constipation being one of the most common symptoms. Low blood pressure upon standing can also occur. DLB commonly causes psychiatric symptoms, such as altered behavior, depression, or apathy. DLB typically begins after the age of fifty, and people with the disease have an average life expectancy, with wide variability, of about four years after diagnosis. There is no cure or medication to stop the disease from progressing, and people in the latter stages of DLB may be unable to care for themselves. Treatments aim to relieve some of the symptoms and reduce the burden on caregivers. Medicines such as donepezil and rivastigmine can temporarily improve cognition and overall functioning, and melatonin can be used for sleep-related symptoms. Antipsychotics are usually avoided, even for hallucinations, because severe reactions occur in almost half of people with DLB, and their use can result in death. Management of the many different symptoms is challenging, as it involves multiple specialties and education of caregivers.

Reference
Wiki: Dementia with Lewy bodies



PTMD IDUniProt AccessionEntrez IDGene NameProtein NameOrganism
PTMD00886P05067351
APP
Amyloid-beta precursor protein precursor protein) [Cleaved into: N-APP; Soluble APP-alpha ; Soluble APP-beta ; C99 ; Amyloid-beta protein 42 ; Amyloid-beta protein 40 ; C83 ; P3; P3; C80; Gamma-secretase C-terminal fragment 59 ) ); Gamma-secretase C-terminal fragment 57 ) ); Gamma-secretase C-terminal fragment 50 ) ); C31]
Homo sapiens
PTMD00338P106364137
MAPT
Microtubule-associated protein tau
Homo sapiens
PTMD00551P194192002
ELK1
ETS domain-containing protein Elk-1
Homo sapiens
PTMD00230P378406622
SNCA
Alpha-synuclein
Homo sapiens
PTMD00041P498412932
GSK3B
Glycogen synthase kinase-3 beta
Homo sapiens
PTMD00671Q1314823435
TARDBP
TAR DNA-binding protein 43
Homo sapiens
PTMD00703Q165551808
DPYSL2
Dihydropyrimidinase-related protein 2
Homo sapiens
PTMD01524P155591728
NQO1
NADH dehydrogenase [quinone] 1 H:quinone oxidoreductase 1)
Homo sapiens
PTMD01568P2734810971
YWHAQ
14-3-3 protein theta
Homo sapiens
PTMD01949Q9Y5A751667
NUB1
NEDD8 ultimate buster 1
Homo sapiens