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CraftArticle describes the relationship of disorders of metabolism to Alzheimer disease and vascular dementia. For 10 years there has been a rapidly increasing number of studies focused on the relationship between metabolic disorders such as diabetes, obesity, hypertension, and insulin resistance and dementia. This review highlights novel or integrative lines of inquiry. Substantiation of the link between metabolic disorders and dementia risk has raised new questions about specific mechanisms underlying these associations that have critical implications for the way we define and classify dementias.
Roth and colleaguesArticle review the role of amylin with leptin in controlling appetite and weight and modulating glucose metabolism and the essential neural pathways mediating these effects. It is a rapidly moving field, and this review will provide an essential explanation for the neurological basis of amylin functions.
Yaffe and colleaguesArticle have found an association between metabolic syndrome and the number of components and risk of developing cognitive impairment in older women. These key observations will now be tested to determine if screening and close management of these at-risk elderly persons would diminish the incidence of cognitive loss.
Kanaya et alArticle report that higher levels of all adiposity measures were associated with worsening cognitive function in men after controlling for metabolic disorders, adipocytokines, and sex hormone levels. Of note, there was no association between adiposity and cognitive change in women.
Fitzpatrick and colleaguesArticle describe differing rates of risk of cognitive loss for midlife and late-life obesity. There is an increased risk in midlife obesity, but the risk estimates reversed in assessments of late-life obesity. These results explain the “obesity paradox.”
Helzner et alArticle find compelling evidence that higher prediagnosis total cholesterol, low-density lipoprotein cholesterol, and diabetes were associated with faster cognitive decline in patients with incident Alzheimer disease.
Qin and colleaguesArticle show that the peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α), a key regulator of glucose metabolism and a potential therapeutic target for therapy for type 2 diabetes, significantly decreased as a function of the progression of Alzheimer disease. Of considerable interest, they have found that increasing PGC-1α expression in Tg2576 neurons attenuates hyperglycemic-mediated β-amyloidogenesis by increasing the nonamyloidogenic α-secretase processing of amyloid precursor protein. These findings are of great interest in linking diabetic metabolic defects to increasing dementia mediated by β-amyloid production.
Jeppesen et alArticle show that during moderate exercise, the balance between fat and carbohydrate use in patients with mitochondrial defects matches that seen in healthy subjects. Thus, manipulating dietary fat and carbohydrate content is not a feasible therapeutic option to improve exercise tolerance in these disorders.
Sonnen et alArticle observed in this elegant study 2 patterns of brain injury with dementia, depending on diabetes mellitus status. These important and novel characterizations of 2 different patterns of cerebral injury in patients, depending on diabetes mellitus status, have etiologic and direct therapeutic implications.
Characteristic pathologic and molecular changes of Alzheimer disease in diabetic and nondiabetic individuals with and without dementia. CAA indicates cerebral amyloid angiopathy; CERAD, Consortium to Establish a Registry of Alzheimer Disease; MFG, middle frontal gyrus; NFT, neurofibrillary tangle; SMTG, superior and middle temporal gyri; *P < .05, compared with the nondementia group with or without diabetes mellitus; †P < .05, compared with the dementia group with or without diabetes.
Brar and colleaguesArticle have determined with 3-T magnetic resonance imaging that there is a significantly greater amount of iron accumulation in the substantia nigra of patients with parkinsonian symptoms. The finding of parkinsonism during the course of Alzheimer disease is associated with iron accumulation.
Giacomini et alArticle provide convincing data supporting the use of magnetization transfer ratio as a practical marker of demyelination and remyelination in acute multiple sclerosis.
Tapiola and colleaguesArticle report that the ratio of cerebrospinal fluid phosphorylated tau to β-amyloid 42 resulted in sensitivity of 91.6% and specificity of 85.7%, with overall accuracy of 90.2% for the presence of neuritic plaque pathology in the brain.
This Month in Archives of Neurology. Arch Neurol. 2009;66(3):298–299. doi:10.1001/archneurol.2009.6
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