MarkesberyArticle reviews the critical evidence for oxidative stress that is an essential ingredient contributing to the cause of Alzheimer disease. Future potential therapy will need to address this issue.
O'Dell and colleaguesArticle outline a thoughtful analysis of how the phenotype of a cell from a diseased individual can be identified and defined through RNA amplification methods. Differences in the pattern of relative messenger RNA levels from damaged and normal cells can provide detailed information about the molecular state of individual cells and patients, leading to potential designer pharmacotherapy in the future. This is a provoking and important concept with obvious potential.
Sabbagh et alArticle provide information on the relationship between choline acetyltransferase activity and synaptic density and clinical progression of Alzheimer disease. The correlations were modest, but the approach is important. WeinerArticle discusses these relationships in a well-focused editorial.
Karitzky and colleaguesArticle describe 9 patients with Kennedy disease and measure regional metabolic abnormalities using proton magnetic resonance spectroscopy. This approach is clinically useful in quantitating metabolic alterations in specific brain areas on a longitudinal basis. Linfante and AshizawaArticle provides a critical analysis of this subject in an accompanying editorial.
Pavlakis and colleaguesArticle measure brain metabolic levels with proton magnetic resonance spectroscopy and correlate these levels with the degree of neonatal asphyxia with Apgar scores. Basal ganglia region metabolic abnormalities correlated best with both the 1- and 5-minute Apgar scores. This suggests a noninvasive means of measuring brain biochemistry in the treatment of critically ill infants.
Chapman et alArticle provide interesting preliminary observations suggesting that the apolipoprotein E genotype may influence disease progression in multiple sclerosis. This is a new area of apolipoprotein E correlation that broadens potential interest in this risk factor.
Tsuang and colleaguesArticle find that the use of apolipoprotein E genotype alone is not helpful in establishing the diagnosis of Alzheimer disease (AD) in the general medical community. They find that although the presence of an ϵ4 allele in older persons with clinical AD increased the probability of having AD, and the absence of an ϵ4 allele in this group decreased the probability of having AD, the association is not strong enough to help clinicians in the differential diagnosis of non-Alzheimer dementia and AD.
Manto et alArticle describe the resetting effects of transcranial magnetic stimulation over the motor cortex on orthostatic tremor associated with cerebellar atrophy. A positive correlation was demonstrated in 3 patients, emphasizing the role of motor cortex in the genesis of orthostatic tremor in a subgroup of individuals.
Worrall and colleaguesArticle describe a mother with amyotrophic lateral sclerosis and her daughter with Creutzfeldt-Jakob disease. Whether these 2 cases occurred in the same family by chance or whether they shared genetic risk factors for the 2 diseases is discussed. The possibility that homozygosity at codon 129 of the prion gene might be a risk factor for amyotrophic lateral sclerosis is put forward.
Kokubo et alArticle provide neuropathologic evidence for inclusions in motor neurons in a Japanese case of amyotrophic lateral sclerosis with a mutation in the SOD-1 gene. Their findings suggest that the inclusions are caused by phosphorylated neurofilaments.
Anderson et alArticle describe a patient with supranuclear facial weakness in association with the one and one-half syndrome and describe in detail the neuroanatomical basis of the lesion.
BrustArticle describes current urban issues in dealing with drug abuse, its neurological consequences, the neurobiological basis of addiction, and our political resolve to address these matters.
This Month in Archives of Neurology. Arch Neurol. 1999;56(12):1439-1440. doi:10.1001/archneur.56.12.1439