Nov 2002
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Nov 2002 international |
IN THIS
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MCI: NATURAL HISTORY AND COSTS
SUSTAINED ACTION
OF
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alzheimer's issues: february 2003 november 2002 august 2002 may 2002 february 2002 november 2001 august 2001 may 2001 february 2001 november 2000 august 2000 june 2000 march 2000 november 1999 may 1999 february 1999 september 1998 june 1998 march 1998 december 1997 |
| EDITORIAL COMMENT |
MCI:
NATURAL HISTORY AND COSTS |
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Natural history of mild cognitive impairment in older persons (NEUROLOGY 2002;59:198-205) |
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To view this abstract in PubMed
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| Primary care expenditures before the onset of Alzheimer's disease (NEUROLOGY 2002;59:573-578) |
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S.M. ALBERT, PHD, MSC, S. GLIED, PHD, H. ANDREWS, PHD, Y. STERN, PHD, ET AL, NEW YORK, NY |
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(NEUROLOGY 2002;58(SUPPL 3):A276) |
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KEVIN PETERS, RONALD SCHOLES, ALAN DONALD, HOWARD FELDMAN, VANCOUVER, BC, MELBOURNE, AUSTRALIA |
Sorry, this abstract is not available |
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(NEUROLOGY 2002;59:1022-1028) |
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| EDITORIAL COMMENT |
A study of the effect
or rivastigmine over one year showed an inhibition of both acetyl- and
butyrylcholinesterase (Darreh-Shori et al). A companion article
by Giacobini et al demonstrated that the level of inhibition of
either enzyme correlates well with performance on a Computerized Neuropsychological
Test Battery. These results along with the evidence from the NORDIC 12-month
placebo-controlled study with donepezil (Winblad et al Neurology
2001;57:489-495, abstract in International Abstracts of November 2001)
demonstrate the sustained benefit of cholinesterase inhibitors over at
least one year.
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Sustained cholinesterase
inhibition in AD patients
(NEUROLOGY 2002;59:563-572) |
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T. DARREH-SHORI, MSC, O. ALMKVIST, PHD, Z.Z. GUAN, MD, PHD, A. GARLIND, MD, PHD, ET AL, STOCKHOLM, SWEDEN, JERUSALEM, ISRAEL |
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Inhibition of
acetyl- and butyryl-cholinesterase in the (J NEURAL TRANSM 2002;109:1053-1065) |
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| EDITORIAL COMMENT |
Strong evidence pointing towards a protective effect of NSAIDs against
AD is again supported by results from the Cache County Study, with a suggestion
that they would be effective if initiated in the years prior to the emergence
of symptoms (Zandi et al ). This protective effect could be explained
by a need for the suppression of the inflammatory response prior to massive
synaptic and cellular losses, which would account for the failure of efficacy
previously shown in randomized studies of anti-inflammatory agents of
already mild to moderate stages of AD. A similar dilemma is facing us
with drugs that will suppress amyloid deposition and plaque formation:
do we establish efficacy in asymptomatic persons at risk (five-year studies),
MCI (three-year studies) or mild to moderate AD (one-year studies)?
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(NEUROLOGY 2002;59:880-886) |
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| EDITORIAL COMMENT |
This superb neuropathological study confirms what most clinicians have
long suspected: The cholinergic deficit in patients with dementia with
Lewy bodies (DLB) is more severe, and occurs earlier in the disease process
compared to patients with Alzheimer's disease. This study provides further
rationale for treating DLB with cholinesterase inhibitors.
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Early and widespread cholinergic losses differentiate dementia with Lewy bodies from Alzheimer disease (ARCH GEN PSYCH 2002;59[10]:946-951) |
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While an intramuscular
preparation of olanzapine is not yet available in Canada, this double-blind,
randomized controlled study compared intramuscular olanzapine to injections
of lorazepam and placebo for the acute management of agitation in elderly
demented patients. Two hours after the first injection both olanzapine
and lorazepam were better than placebo, though after 24 hours, only olanzapine
was superior to placebo. All treatments were well tolerated with no significant
adverse events more common in the active treatments compared to placebo.
Even without the availability of intramuscular olanzapine, this study
lends some support to the common practice of using lorazepam as a prn
agent for acute agitation in dementia
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(NEUROPSYCHOPHARMACOLOGY 2002;26[4]:494-504) |
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There
has been on-going debate on whether depression earlier in life predisposes
an individual to dementia. In a large prospective longitudinal study, elderly
Catholic clergy members without dementia were followed for seven years.
Depression scale scores were both positively associated with the risk of
developing AD as well as the rate of cognitive decline.  |
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(NEUROLOGY 2002;59:364-370) |
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R.S. WILSON, PHD, L.L. BARNES, PHD, C.F. MENDES DE LEON, PHD, N.T. AGGARWAL, MD, ET AL, CHICAGO, IL, PHILADELPHIA, PA |
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Depressive
symptoms and syndromes in patients with AD are common serious problems that
have a negative functional and cognitive impact beyond the burden of the
dementia. In a series of important articles, the concept of depression in
AD is reviewed and provisional diagnostic criteria are suggested. |
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(PSYCHIATRY 2002;52:243-252) |
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CONSTANTINE G. LYKETSOS, JASON OLIN, BETHESDA, BALTIMORE, MD |
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(AM J GERIATR PSYCHIATRY 2002;10:125-128) |
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| Provisional diagnostic criteria for depression of Alzheimer disease: rationale and background (AM J GERIATR PSYCHIATRY 2002;10:129-141) |
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JASON T. OLIN. PHD, IRA R. KATZ, MD, PHD, BARNETT S. MEYERS, MD, LON S. SCHNEIDER, MD, ET AL, BETHESDA, ROCKVILLE, MD |
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COGNITIVE PHARMACOTHERAPY OF ALZHEIMER'S DISEASE AND OTHER DEMENTIAS |
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