Patrick L. McGeer

Descending projections of the basal forebrain in the rat demonstrated by the anterograde neural tracer Phaseolus vulgaris leucoagglutinin (PHA-L)

Descending pathways from the mediobasal forebrain were studied in the rat by injecting anterograde axonal tracer Phaseolus vulgaris leucoagglutinin into the substantia innominata and diagonal band of Broca. From both areas, positive fibers which varied in density were observed in the mediodorsal and ventral parts of the ventroposterior and ventromedial thalamic nuclei, the lateral habenula, the stria medullaris, the lateral hypothalamus and the ventral tegmental area. This descending complex appeared predominantly course through the medial forebrain bundle from which positive fibers ramified into the fasciculus thalamicus to distribute in the thalamic nuclei. A minor descending pathway through the stria medullaris was also noted which terminated in the lateral habenula and the mediodorsal thalamic nucleus. An obvious difference in terminal distribution in the medial habenula, mediodorsal thalamic nucleus and pons could be observed following substantia innominata or diagonal band injection.

Acidic fibroblast growth factor-like immunoreactivity in brain of Alzheimer patients

Localization of acidic fibroblast growth factor (aFGF)-like immunoreactivity was examined in postmortem human brain tissue of Alzheimer and age-matched control cases using a rabbit polyclonal antibody specific for aFGF. In control cases, a small number of glial cells were stained very weakly in white but not in gray matter. In Alzheimer cases, some astrocytes were strongly stained for aFGF in both gray and white matter. These intensely staining cells were frequently observed surrounding senile plaques, but represented a small proportion of the total astrocytic population. The present study suggests that aFGF may be upregulated in areas of Alzheimer pathology.

Anti-inflammatory agents as possible protective factors for Alzheimer’s disease: Analysis of relevant epidemiological studies

Alzheimer’s disease (AD), an intractable disorder which primarily affects the elderly, is the cause of more than two-thirds of all dementia cases. Currently available drugs may give some symptomatic relief but are not designed to prevent the disease or arrest its progression. As reviewed elsewhere in this book, many studies have now shown the presence of a chronic inflammatory reaction in affected regions of AD brain. Particularly noteworthy is the presence of many activated microglia and greatly elevated levels of inflammatory cytokines and all the components of the classical complement cascade, including the membrane attack complex. This complex, as well as free radicals and other molecules produced in abundance by activated microglia, may damage host tissue. This has led to the hypothesis that antiinflammatory agents may slow the progress of AD or inhibit its onset [1 2].