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Brain protein was lower in mouse models of memory problems

Compared with controls, mouse models of Alzheimer’s disease, diabetes-related brain impairment and brain aging had less of a protein that helps organize nerve-cell connections.

Paper by Husileng Hai, Yifang Luo, Jiale Ren, +2 more authorsZhen Yang · Tianjin University of Traditional Chinese Medicine
Figure 4. BAIAP2 expression is reduced in the hippocampal CA1, CA3, and dentate gyrus regions of AD, DE, and aging model mice.(A) Representative immunofluorescence images of BAIAP2 in the hippocampal CA1,…
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Figure 4. BAIAP2 expression is reduced in the hippocampal CA1, CA3, and dentate gyrus regions of AD, DE, and aging model mice.(A) Representative immunofluorescence images…BAIAP2 expression is reduced in the hippocampal CA1, CA3, and dentate gyrus regions of AD, DE, and aging model mice.(A) Representative immunofluorescence images of BAIAP2 in the hippocampal CA1, CA3, and dentate gyrus (DG) regions from control, Alzheimer’s disease (AD), diabetic…Hai et al.

Our read

Mechanisms
Studied:
Preprint: experiments in mice modeling cognitive impairment, against control mice
What changed:
Hippocampal BAIAP2 protein levels were lower in mice modeling memory problems than in control mice
The catch:
Memory effects of directly changing BAIAP2 levels were not measured
In the record:
One of 17 papers on amyloid-beta on record: 3 with results in people, 6 in animals.
Why it’s aging research:
Biological age, frailty, function, multimorbidity or death.

Editor of record: Boris Djordjevic · AgingResearch.News

Paper
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Mice modeling Alzheimer’s disease, diabetes-related brain impairment and brain aging showed problems remembering locations in animal experiments. Compared with controls, all three model groups had lower levels of BAIAP2, a protein that helps organize nerve-cell connections, in the hippocampus, a brain region involved in memory. Activity of the gene encoding this protein was also lower.

The researchers first analyzed gene activity in individual cells from three existing datasets. BAIAP2 was the only shared central gene in networks of nerve-cell gene activity associated with the three conditions. In separate experiments, nerve-like cells grown in the lab also had lower BAIAP2 gene activity and protein levels after exposure to stimuli used to mimic Alzheimer’s disease, metabolic stress or aging-related damage.

Why it matters

Brain aging and these disorders share damage to nerve-cell connections. The authors propose BAIAP2 as a potential common target for strategies against cognitive decline.

Caveats

The experiments did not test whether changing BAIAP2 caused or corrected memory problems; lower levels could accompany rather than cause the impairment. The work is a preprint and has not yet been peer-reviewed.

Where the evidence stands

Cellular senescence

Cells, worms or flies, mice and humans: replicated by independent labs.

C, W, M, H: cells, worms or flies, mice, humans. Dark: independent labs found the same change there. Light: one lab or one study. Outline: nothing yet.

Labs are independent when their papers share no last author and no institution.

Against: findings that point the other way from most findings on the same outcome.

No results posted: trials that ended over a year ago with no results on ClinicalTrials.gov and no paper reporting them.

Company ties: findings with an author at a company, or from a paper whose competing-interests statement declares ties to one.

Includes the processes named after it and trials of drugs aimed at it.

  • 854 independent labs in 75 countries
  • 515 findings against
  • 51 trials, 15 with no results posted
  • Funders: National Natural Science Foundation of China and others
  • 663 of 9,839 findings with company ties
  • 49 of 51 trials sponsored by developers of drugs aimed at it

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