@GABAergic deafferentation hypothesis of brain aging and Alzheimer's disease; pharmacologic profile of the benzodiazepine antagonist, flumazenil (Marczynski 1995)

2022-01-14 links: GABA Alzheimer’s See also:

• GABAergic deafferentation hypothesis of brain aging and Alzheimer’s disease revisited (Marczynski, 1998)
• Chronic administration of flumazenil increases life span and protects rats from age-related loss of cognitive functions: a benzodiazepine/GABAergic hypothesis of brain aging (Marczynski et al., 1994)
• Altered glial–neuronal crosstalk: Cornerstone in the pathogenesis of hepatic encephalopathy
• Perinatal upregulation of benzodiazepine receptor ontogenesis: “fearless” and more efficient goal-directed behavior of adult rat progenies
• The space where aging acts: focus on the GABAergic synapse

@GABAergic deafferentation hypothesis of brain aging and Alzheimer’s disease; pharmacologic profile of the benzodiazepine antagonist, flumazenil (Marczynski, 1995) #

• The gabaergic deafferentation hypothesis proposes that increasing gabaergic tone through lifespan promotes transcriptional drift and a general decline in gabaergic interneuron binding affinities and with it a decline in gabaergic interneurons which precedes excitotoxic glutamatergic deafferentation and reduced insulin sensitivity in the brain through increased amyloid beta production as Insulin Degrading Enzyme activities are greatly reduced. A benzodiazepine receptor = GABA-A, for that’s where they bind to enhance the effects of GABA. Might just be an archaic term?

• Flumazenil treatment lead to significantly higher scores for ambulation and exploratory behavior. Made significantly less working memory and reference memory errors, relative to 25-month-old control group.