I was delighted to be invited to listen to Malila, the youngest Nobel Prize winner for her advocacy of education for girls throughout the world. Education is indeed the best way to solve the problems that bedevil any society, especially the education of the hands that rock the cradle.
Consider two vexing problems: obesity and neurodegeneration (see previous blog). They are, like all problems, associated with a lack of education.
Analysis identifies factors that may explain differences in cognitive ability among older adults
NBC News (2/11, Carroll) reported “a handful of factors, such as education, income and job type, may increase the likelihood that people in their mid-50s will still be mentally sharp,” according to “an analysis of data from more than 7,000 U.S. adults” who “were 54 to 65 years old in 1996 and then 20 years later.” The results published in PLOS One “showed that these factors could explain nearly 40% of the differences in the amount of cognitive ability people had lost by age 54.” According to researchers, “education, in particular whether a person had finished college, made the biggest difference in cognitive abilities such as memory, judgment and focus.”
Lower quality education increases dementia risk
Healio Minute, February 16, 2023. Data derived from Soh Y, et al. JAMA Neurol. 2023;doi:10.1001/jamaneurol.2022.5337.
Education quality was associated with dementia risk later in life, according to findings published in JAMA Neurology. Yenee Soh, ScD, a postdoctoral research fellow at Kaiser Permanente Northern California in Oakland, and colleagues noted that lower quality education was more common among Black people and may be a contributor to racial disparities in dementia.
“Higher educational quality (eg, teacher salaries, student-teacher ratio, term length) has been found to be associated with higher educational attainment and higher earnings, which in turn can contribute to protective health behaviors for dementia prevention,” Soh and colleagues wrote. “Structural racism decreases investment in schools that serve Black children and limits access to high-quality education and opportunities for educational advancement, a stark example being the history of Jim Crow laws in the U.S. South that segregated schools for Black and white children.”
Gut microbes modulate neurodegeneration
J. Science 2023;379:142
“Amyloid-β (Ab), tau, and apolipoprotein E (APOE) are major players in the pathogenesis of Alzheimer’s disease (AD), which involves neuroinflammation and neurodegeneration (1). Recently, gut microbes have emerged as an important factor implicated in neurodegeneration (2). However, how gut microbes interplay with APOE and tau remains elusive. On page 155 of this issue, Seo et al. (3) investigate tau-mediated neurodegeneration using mouse models in which animals were raised conventionally and in germ-free (GF, lacking all microbiota) conditions. They demonstrate that gut bacteria play a causative role in tau-mediated neurodegeneration through modulation of inflammation in the periphery and the central nervous system (CNS). This neuroinflammation arose in an APOE isoform–dependent and sex-specific manner.”
Comment: microbiota is heavily influenced by our diet, and vice versa.
Is Alzheimer’s disease a Type 3 Diabetes? A critical appraisal
J. Biochimica et Biophysica Acta (BBA) – Molecular Basis of Disease 2017;1863:1078
Recently researchers proposed the term ‘Type-3-Diabetes’ for Alzheimer’s disease (AD) because of the shared molecular and cellular features among Type-1-Diabetes, Type-2-Diabetes and insulin resistance associated with memory deficits and cognitive decline in elderly individuals. Recent clinical and basic studies on patients with diabetes and AD revealed previously unreported cellular and pathological among diabetes, insulin resistance and AD. These studies are also strengthened by various basic biological studies that decipher the effects of insulin in the pathology of AD through cellular and molecular mechanisms. For instance, insulin is involved in the activation of glycogen synthase kinase 3β, which in turn causes phosphorylation of tau, which involved in the formation of neurofibrillary tangles. Insulin also plays a role in the formation amyloid plaques. In this review, we discussed significant shared mechanisms between AD and diabetes and we also provided therapeutic avenues for diabetes and AD.
