Hussein N. Yassine

How the White House used studies with ‘weak’ evidence to tie Tylenol to autism Experts say White House presented ‘association as causation’ and based conclusions on ‘poor quality studies’

www.theguardian.com/us-news/2025...
A good analysis by the Guardian explaining how associations are often not causations. Love the heat and Ice cream analogy..

At human doses? Sorry did not look closely
A problem with many mice studies is doses used are quite exaggerated by design to see an effect.

I don’t think anyone paid attention to this paper until now. A meta analysis can be useful if the papers they are citing are credible and the authors follow proper methodology. Without a mechanism, the association of Tylenol with autism is vague. This paper makes us look more deeply into this.

Enjoyed your podcast! Appreciated the insights into education and cognition.

Very beautiful Meredith!

Well said! Science is for all of us and should be above politics.

Microglial States Are Susceptible to Senescence and Cholesterol Dysregulation in Alzheimer's Disease Senescent microglia in Alzheimer's disease exhibit dysregulated cholesterol metabolism and express Disease-Associated Microglia (DAM) signatures, including inflammatory and phagocytic markers. Single....

This study, led by the talented grad student Boyang Li, identifies microglia undergoing cellular senescence in AD, and targeting cholesterol metabolism in senescent microglia is a therapeutic approach to slow AD progression. onlinelibrary.wiley.com/doi/10.1111/...

Women with Down syndrome may develop Alzheimer's disease more rapidly than men UC Irvine study finds sex differences may impact treatment approaches

news.uci.edu/2025/08/12/w...
Great work by a fantastic team!

Women with Down syndrome may develop Alzheimer's disease more rapidly than men UC Irvine study finds sex differences may impact treatment approaches

Women with Down syndrome may develop Alzheimer's disease more rapidly than men news.uci.edu/2025/08/12/w... by @ucirvine.bsky.social

#Alzheimers #dementia #DownSyndrome #WomensHealth @elizabethhead.bsky.social

SNAP program in vulnerable groups more effective in lowering cognitive decline than the more expensive intensive lifestyle intervention in the general population

Don't miss out on poster presentations by #NIAfundedADRC REC scholars today at #AAIC2025!

Learn more about the Research, Education, Component (REC) and REC scholars: naccdata.org/adrc-resourc...

Congratulations to @sdukehan.bsky.social for leading a major gerontology journal

The system can be gamed
Reviews are highly cited and often self citing the authors work
Unfortunately we all do this
Both journals and authors can inflate their citation indices with paper mills or high IF reviews
The number of citations does not replace a critical appraisal

Someone who kept citing himself..

Letrozole and irinotecan are not typically used for aging-related diseases. These are chemotherapies with severe side effects. While the approach is novel, the results are unconventional to say the least!

Congratulations! There is light at the end of the tunnel

Fantastic work by a fantastic team!

Increased cerebrospinal fluid and plasma apoE glycosylation is associated with reduced levels of Alzheimer’s disease biomarkers - Alzheimer's Research & Therapy The apolipoprotein E (APOE) ε4 allele is the strongest genetic risk factor for late-onset Alzheimer’s disease (AD). ApoE is glycosylated with an O-linked Core-1 sialylated glycan at several sites; how...

Congratulations to Dobrin Nedelkov and Zoe Tsokolas! We demonstrate that apoE glycosylation in CSF predicts tau pathology in the ADNI cohort. We identify a new role for sugars attached to apoE in AD. Could less glycosylated apoE play a major role in tau spread? link.springer.com/article/10.1...

Perhaps the problem as you note is an incomplete understanding of how science works. Selection bias is one, but there are many others. Interpretation of study designs, limitations, conflating causation with associations. This can be fixed if children were exposed to critical thinking early on.

Terrible!

We are all in the same boat. We just have to keep going.

Any tips? I deleted X…

4/4: When we lowered oxysterols using cyclodextrin in vivo, ABCA1 recycled to the plasma membrane, and neuroinflammation was reduced. Accumulation of oxidized cholesterol in lysosomes in APOE4 AD is an important mechanism for senescence. Drugs targeting lysosomal lipids are promising strategies.

3/4: Proteomic discovery experiments identified the cholesterol sensor, Caveolin-1 as the mechanism for ABCA1 sequestration into lysosomes. The accumulation of oxysterol species in APOE4 induced ABCA1 and trapped it in lysosomes.

2/4: We previously identified that APOE4 traps ABCA1 in lysosomes of cell and animal models. In agreement, we found more ABCA1 in lysosomal fractions isolated from post-mortem brain tissue samples compared with controls, indicating that more ABCA1 is sequestered into lysosomes with APOE4 AD.

1/4: We observed a paradoxical increase in ABCA1 expression in APOE4 brain tissues with AD compared to controls. Increased ABCA1 expression was associated with cellular senescence. This led us to question whether increased ABCA1 expression translated into better ABCA1 cholesterol efflux function.

Cellular senescence induced by cholesterol accumulation is mediated by lysosomal ABCA1 in APOE4 and AD - Molecular Neurodegeneration Background Cellular senescence, a hallmark of aging, has been implicated in Alzheimer’s disease (AD) pathogenesis. Cholesterol accumulation is known to drive cellular senescence; however, its underlyi...

Is making brain HDL by inducing ABCA1 a viable strategy for APOE4 Alzheimer's? Our talented researcher Dr. Shaowei Wang has looked deeply into this question over the past 6 years, and the work has finally been published 1/4: molecularneurodegeneration.biomedcentral.com/articles/10....

4/4: Lowering oxysterols lowered markers of cellular senescence, implicating ABCA1 enriched lysosomes in mTOR activation and cellular senescence.

3/4: Using a proteomic approach, we discover that APOE4 traps ABCA1 in lysosomes by upregulating caveolin-1, a cholesterol sensor. When we lowered oxysterols by cyclodextrin, we enhanced the recycling of ABCA1 to the plasma membrane.

2/4: We previously identified that APOE4 traps ABCA1 in lysosomes in cell and animal models. We extend this observation here into human brain tissues. More ABCA1 expressed in APOE4 AD is trapped in lysosomal fractions.