New Potential Therapy For Frontotemporal Dementia
Frontotemporal disorders tin move survive grouped into iii types defined past times the earliest symptoms: progressive behavior/personality decline, progressive linguistic communication decline, in addition to progressive motor skills decline.
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- Frontotemporal dementia, known every bit FTD, is a devastating illness inwards which patients convey rapid in addition to dramatic changes inwards behavior, personality in addition to social skills.
- The historic menstruum of onslaught for FTD is relatively young, commonly hitting patients inwards their mid- to belatedly 50s.
- The prognosis is grim; patients apace deteriorate in addition to commonly top inside 10 years later onset. Currently, at that spot is no effective handling for FTD.
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- The UAB query team’s endeavor focused on mutations inwards sure enough genes, primarily inwards the Microtubule Associated Protein Tau gene.
- An accumulation of tau poly peptide is associated amongst Alzheimer’s disease, the nigh mutual shape of dementia; only piddling is known how tau mutations impact specific encephalon regions in addition to drive FTD.
- The UAB researchers used a novel mouse model expressing human tau amongst an FTD-associated mutation.
- These mice demonstrate physical behaviors like to those seen inwards humans amongst FTD — compulsive, excessively repetitive actions such every bit grooming, for example.
- The mice every bit good had impaired synaptic in addition to network component division inwards sure enough encephalon network regions.
Frontotemporal dementia, known every bit FTD, is a devastating illness inwards which patients convey rapid in addition to dramatic changes inwards behavior, personality in addition to social skills. The historic menstruum of onslaught for FTD is relatively young, commonly hitting patients inwards their mid- to belatedly 50s.
“We flora that mutant tau impairs synapses — the connections betwixt neurons — past times reducing the size of the anchoring sites of an essential glutamate receptor called NMDA,” said Erik Roberson, M.D., Ph.D., associate professor inwards the Department of Neurology in addition to main investigator for the study. “Reduction of the anchoring sites left fewer NMDA receptors available at the synapse to have excitatory signals, thence limiting synaptic firing in addition to network activity.”
- The squad in addition to so employed cycloserine, a drug already approved for work past times the FDA, which is known to help NMDA receptor function.
- This boost of NMDA receptor component division was able to restore synaptic firing in addition to thereby restore network activity inwards the fauna model.
- The restoration of normal network activity reversed the behavioral abnormalities seen inwards the mice.
“This written report provides mechanistic insight into how a tau mutation affects specific encephalon regions to impair a network,” said Roberson. “It every bit good provides a potential therapeutic target, the NMDA receptor, which appears to right the network in addition to behavioral abnormalities.”Roberson’s squad hypothesizes that increasing NMDA receptor component division may create goodness human FTD patients. With farther preclinical validation, this hypothesis could survive tested inwards clinical trials using the already available drug cycloserine.
Source UAB News
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