Volume 1, Number 1, March 1998
Pages 1-34
Paul Averback, David Morse, Hossein Ghanbari
Bursting Dense Microspheres (Spherons) in Alzheimer's Disease: A
Review of Studies (1980-1997) on Spherons and the Pathogenesis of
Alzheimer's Disease
Abstract: This paper reviews our research studies during the past
17 years on the relationship of cerebral protein dense microspheres
(DMS), termed spherons, and senile plaques (SP) in the aged human
brain and in AD. Initially, correlative anatomical and pathological
data suggested that spherons may evolve into SP. This led to
morphometric studies which strongly supported theory. Biochemical
studies were undertaken which showed that spherons could be isolated
to homogeneity from brain tissue and contained the markers
associated with SP. Experiments in vitro with spherons, and with
inoculation of spherons into animals, reproduced SP lesion
characteristics. To test the validity of using spherons for drug
screening, experimental drugs were tested, a few of which are
capable of blocking the formation of spheron-induced experimental
SP.
Pages 35-44
Xue-Qing Chen, John R. Fawcett, Yueh-Erh Rahman, Thomas A. Ala and
William H. Frey II
Delivery of Nerve Growth Factor to the Brain via the Olfactory
Pathway
Abstract: Purpose. To assess the potential of delivering nerve
growth factor (NGF) to the brain along the olfactory neural pathway
for the treatment of Alzheimer's disease. Methods. Recombinant
human NGF (rhNGF) was given as nose drops to anesthetized rats.
The rhNGF concentrations in the brain were determined by
enzyme-linked immunosorbent assay (ELISA). Results. Following
olfactory administration, rhNGF reached the brain within an hour,
achieving a concentration of 3400 pM in the olfactory bulb, 660-2200
pM in adjacent brain regions and, 240 pM and 180 pM in the
hippocampus and the amygdala, respectively. In contrast, little or
no rhNGF was found in the brain following intravenous
administration. Conclusions. A significant amount of rhNGF can be
delivered to the brain via the olfactory pathway. The detection of
rhNGF by ELISA indicates that rhNGF is delivered to the brain
relatively intact. The rapid appearance of rhNGF in the brain
suggests that it may be transported by an extraneuronal route into
the brain via intercellular clefts in the olfactory epithelium.
Further work to clarify the transport mechanism is underway. The
olfactory pathway is a promising, non-invasive route for drug
delivery to the brain, which has potential for the treatment of
neurodegenerative diseases including Alzheimer's disease.
Pages 45-55
George Perry, Rudy J. Castellani, Keisuke Hirai and Mark A. Smith
Reactive Oxygen Species Mediate Cellular Damage in Alzheimer
Disease
Abstract: The two most striking features of Alzheimer disease are
(i) the multitude of abnormalities affecting essentially every
system and (ii) the strict age dependence. Recent work suggests
that both features are linked to increased oxidative stress that
dames lipids, proteins and nucleic acids and results in redox-active
metal accumulations, mitochondrial damage and formations of advanced
glycation endproducts. Interesting, ß-protein precursor, amyloid-ß,
presenilins, and apolipoprotein E have all been linked to reactive
oxygen species production or apoptosis, a process intimately
associated with oxidative stress. In therapeutics, the commonality
between a number of efficacious agents appears to be oxidative
stress reduction. Therefore, we contend that oxidative stress is
the element that links the multitude of changes in Alzheimer disease
and that a reduction of oxidative stress will have a dramatic effect
on reducing the incidence or progression of Alzheimer disease.
Pages 57-59
William K. Summers
Bismuth Toxicity Masquerading Alzheimer's Dementia
Abstract: A 76-year-old white married female had rapid onset dementia
with myoclonus and was admitted to an HMO hospital where she was initially
diagnosed as Alzheimer's disease. The physician-husband suggested
that the condition might be due to the Pepto-Bismol which she had taken
chronically to control her irritable bowel syndrome. An elevated
serum bismuth level of 242 mg/L (normal is 65 mg/L) established bismuth
toxicity as the cause of the dementia. With treatment the patient
returned to a normal mental state. The possibility of bismuth encephalopathy
needs to be considered in the differential diagnosis of possible Alzheimer's
dementia.
RETURN
TO INDEX
top |