Salk Institute researchers surveyed human embryonic kidney cells and skin biopsy-derived fibroblasts from Alzheimer’s patients to identify proteins involved in regulating mitochondrial stress—a hallmark of aging. The newly identified proteins could one day serve as biomarkers to screen for in skin biopsies, simplifying diagnosis and assessment of Alzheimer’s disease.

To study early-life changes in fAD brain cells, researchers including Zhen-Ge Luo and colleagues from ShanghaiTech University, China, have leveraged stem cell-derived brain organoids, to model aspects of early human brain development and function in the laboratory. Their work was published today in Stem Cell Reports.  Organoids derived from fAD patients recapitulated AD-specific features such as increased amyloid protein, contained less mature neurons, and had higher cell death rates than healthy organoids. fAD organoids also had distinct changes in gene expression. One of the genes of note is TMSB4X which makes an anti-inflammatory protein called Thymosin β4 (Τβ4). Interestingly, like in the brain organoids, TMSB4X expression was also reduced in neurons of post-mortem AD patients brain samples.

The Korea Research Institute of Standards and Science (KRISS, President Lee Ho Seong) has developed a diagnostic platform that amplifies the unique optical signals of molecules by more than a hundred million times, enabling the precise detection and quantification of trace amounts of Alzheimer’s disease biomarkers in body fluids.

For decades, Alzheimer’s disease (AD) research has focused on its visible villains—amyloid plaques and tau tangles. But beneath the surface, another player may be quietly steering the disease’s course: lipid metabolism. Lipids, the essential substances that build and fuel the brain, are proving to be powerful influencers of disease progression. When their balance falters, harmful proteins accumulate, synapses weaken, and inflammation spreads. This new review pulls together cutting-edge findings that link genetic risk factors, like APOE4, to disrupted cholesterol transport, faulty fat storage, and poor lipid clearance—unveiling a hidden layer of AD biology and pointing toward untapped therapeutic strategies.