A Putrid Problem: Astrocytic Urea Cycle in Alzheimer’s?
Aβ revs up urea metabolism in astrocytes, producing an intermediate that is converted into the neurotransmitter GABA. This dampens synaptic transmission and blunts memory in mice.
NEWS
Astrocyte-to-Neuron Conversion Questioned
A spate of recent studies could not replicate the finding that knocking down the RNA-binding protein PTBP1 in astrocytes triggers their conversion to neurons. Leaky expression of the knockdown construct in endogenous neurons may be to blame.
Destined to Decline: Plaque-Tangle Combo Foretells Impairment
Cognitively normal people with PET evidence of both hallmark Alzheimer's lesions slid toward MCI or dementia within about three years. Their risk of this decline was 19-fold higher that of people without these deposits.
Astrocyte Reactivity: Opposing States Emerge
Astrocytes react differently depending on the type of insult or injury inflicted upon the brain. Two studies identified transcriptional regulators controlling astrocyte responses.
Digital Tools Abound, Yet Remote Biomarkers for FTD Remain Exploratory
At the inaugural Holloway Summit hosted by AFTD, researchers, regulatory, and foundation leaders discussed how to advance digital tools from the idea stage into standardized, reliable form for diagnosis and trials.
Digital Biomarkers of FTD: How to Move from Tech Tinkering to Trials?
The development of digital health technologies and biomarkers to track the progression of FTD’s myriad manifestations was the focus of the first Holloway Summit.
C1q Shows Promise as Therapeutic Target to Stop Synapse Loss
A C1q antibody hit its target in a small Phase 2 Huntington’s trial, while indirect inhibition of C1q restored synaptic density in Alzheimer’s model mice.
TMEM175 Maintains Lysosome pH by Pushing Out Protons
While TMEM175 ushers potassium ions out of neutral lysosomes, it shuttles protons out of acidic ones. Sans TMEM175, lysosomes become too “tart,” and stop working. Two papers say so.
SPOTLIGHT
Destined to Decline: Plaque-Tangle Combo Foretells Impairment
Having both amyloid plaques and tau tangles destines a cognitively intact person to decline within the next few years. Cognitively normal adults with plaques and tangles declined faster than those without either pathology, and faster than those with only plaques. Over 3.5 years, people with plaques and tangles had 15 to 20 times higher risk of developing mild cognitive impairment or dementia.
Greasing the Wheels to Digital Biomarkers for FTD
Changes in activity, speech, sleep, or the way a person moves are all examples of measurements that can be captured remotely using digital tools. If transformed into digital biomarkers, such remote measures could dramatically improve diagnosis and the testing of potential treatments in FTD. At the inaugural Holloway Summit held in Miami last month, leaders in FTD research, industry, foundations, and technology discussed how to transform the tools already available into standardized digital biomarkers.
TMEM175 Maintains Lysosome pH by Pushing Out Protons
Lysosomes require tight regulation of their pH to digest their contents. Researchers know that V-ATPase pumps protons into these little sacs, but what protein shuttles the ions back out? Researchers now point to TMEM175, the potassium channel already known as a risk gene for Parkinson’s disease and Lewy body dementia. TMEM175 shunts potassium out of lysosomes when they are neutral, but switches to protons once they become too “sour.” TMEM175 knockout cells have hyperacidified lysosomes and hobbled hydrolases. The work highlights how too much acidification can be as bad as too little.
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