Persons with dementia live an estimated four-and-a-half years after diagnosis, according to a study in the January 10 BMJ. More than 13,000 people 65 and older were assessed for dementia at regular intervals from 1991 to 2005. Of the 438 participants who developed dementia during the study period, 356 (81%) died, with a median survival time from diagnosis of dementia of 4.1 years for men and 4.6 years for women. Median survival time also decreased with patient age: 10.7 years for the age-group 65 to 69, 5.4 years for the age-group 70 to 79, 4.3 years for the age-group 80 to 89, and 3.8 years for those 90 and older. Sex, age of onset, and disability significantly predicted mortality in the presence of dementia. The authors suggested that survival estimates can be used for prognosis and planning for patients, caregivers, service providers, and policy makers.

Statins were not linked to incident Alzheimer’s disease or to disease pathology in a study reported in the January 16 online Neurology. About 18% of 929 Catholic clergy (68.7% women; mean baseline age, 74.9) free of dementia at the beginning of the study used statins at some point before their death, at which time a brain autopsy was performed. Statin use was not related to global Alzheimer’s disease pathology, tangles, or infarction, although statin users were less likely to have amyloid, noted the researchers. One hundred ninety-one participants developed Alzheimer’s disease during the study; however, statin use at baseline (12.8%) was not associated with the disease, nor was it associated with changes in global cognition or in five separate cognitive domains.

Rapid cognitive improvement occurred within minutes following perispinal administration of etanercept in an 81-year-old man with late-onset Alzheimer’s disease, reported researchers in the January 9 Journal of Neuroinflammation. Interspinous injection of 25 mg of etanercept was given at the C6-7 interspace, followed by Trendelenburg positioning with the head dependent for five minutes. At 10 minutes, the patient was “noticeably calmer, less frustrated, and more attentive” and was able to identify the state and year, according to the authors. The patient remained “markedly clinically improved throughout the week” following treatment, they added. The researchers suggested that the improvement was caused by the amelioration of the effects of excess tumor necrosis factor a on synaptic mechanisms in Alzheimer’s disease.

t-PA is required to facilitate neuronal nitric oxide release for increased blood flow to the brain following somatosensory stimulation, as reported in the January 22 Proceedings of the National Academy of Sciences. “t-PA controls N-methyl-D-aspartate–dependent nitric oxide synthesis by influencing the phosphorylation state of neuronal nitric oxide synthase” but does not enhance the currents or the associated intracellular rise in Ca2+, said the study authors. The investigators suggested that this previously unrecognized role of t-PA may have implications in the treatment of Alzheimer’s disease and stroke, both of which have been associated with marked declines in natural brain levels of the enzyme.

Exposure to trichloroethylene may increase a person’s risk for parkinsonism, reported researchers in the December 21, 2007, online Annals of Neurology. Thirty industrial coworkers had long-term (eight to 33 years) exposure to trichloroethylene. Three workers who were positioned closest to the trichloroethylene source and were subjected to chronic inhalation and dermal exposure from handling metal parts soaked in trichloroethylene had Parkinson’s disease. The remaining workers were distant from the trichloroethylene source but experienced chronic respiratory exposure; they showed many signs of parkinsonism, including significant motor slowing. In accompanying animal studies, the research team demonstrated that oral administration of trichloroethylene for six weeks “instigated selective complex 1 mitochondrial impairment in the midbrain with concomitant striatonigral fiber degeneration and loss of dopamine neurons.”

Elevated levels of serum triglycerides and non-HDL cholesterol were associated with large artery atherosclerotic stroke, according to a study published in the December 26, 2007, online Neurology. Of 1,049 patients admitted to a single university medical center with ischemic stroke or transient ischemic attack during a four-year period, those with large artery atherosclerotic stroke (23.5%) had significantly higher levels of total cholesterol, triglycerides, LDL cholesterol, and non-HDL cholesterol versus those with non–large artery atherosclerotic, non–small vessel disease (55%); triglyceride-to-HDL cholesterol ratio was also significantly higher. Patients in the uppermost quartiles of triglycerides and non-HDL cholesterol had odds ratios for large artery atherosclerotic stroke of 2.69 and 2.39, respectively, compared with patients in the lowest quartiles. The investigators noted that LDL cholesterol was not associated with stroke risk, however.

There is no evidence of a recent decrease in autism in California despite the exclusion of more than trace levels of thimerosal from nearly all childhood vaccines, as reported in the January Archives of General Psychiatry. Exclusion of thimerosal from childhood vaccines in the United States occurred between 1999 and 2001, stated the researchers, who analyzed California Department of Developmental Services autism client data from January 1, 1995, to March 31, 2007. The estimated prevalence of autism for children at each year of age from 3 to 12 increased throughout the study period and increased in children ages 3 to 5 for each quarter. Since 2004, the absolute increase and rate of increase in children ages 3 to 5 with autism were higher than those among children of the same ages with any eligible condition, including autism.

The deletion or duplication of a segment on chromosome 16p11.2 may account for 1% of all autism cases, according to a report in the January 9 online New England Journal of Medicine. A complete genome scan of 751 multiplex families with autism culled from the Autism Genetic Research Exchange (AGRE) revealed a de novo 593 kb deletion in five instances. The identical deletion was evident in five of 512 children referred for developmental delay, mental retardation, or suspected autism spectrum disorder and in three of 299 persons with autism in an Icelandic population, reported researchers; two unscreened control participants in the Icelandic cohort also had the deletion, however. A reciprocal duplication of the region “occurred in seven affected persons in AGRE families and four of the 512 children …[and] appeared to be a high-penetrance risk factor,” added the authors.

The cancer drug bryostatin may enhance the building and rewiring of structural storage sites for long-term associative memory, according to the results of a study in the December 4, 2007, Proceedings of the National Academy of Sciences. Researchers analyzed the single dendritic spines of CA1 pyramidal cells in the hippocampi of water maze–trained and control rats. Two days after training, there was a memory-specific increase in the number of mushroom spines that was enhanced by the PKC activator bryostatin and impeded by a PKCa-isozyme blocker, reported the authors. Mushroom spine increase was also accompanied by increased numbers of “perforated” postsynaptic densities and presynaptic vesicles and increased occurrence of double-synapse presynaptic boutons. The researchers suggested that the findings may be applicable in human conditions such as Alzheimer’s disease, in which brain synapses are destroyed.

NR