Læknablaðið : fylgirit - 01.05.2002, Qupperneq 34

ABSTRACTS / 3 3RD SNC & 2N° SCNN
one hand the cognitive impairment and on the other the psychiatric
and behavioral symptoms of the disease (BPSD: Behavioral and
Psychological Symptoms in Dementia). Among the psychiatric
symptoms are depression, anxiety, paranoia and hallucinations and
the behavioral symptoms may include agitation, irritability, restless-
ness, wandering and screaming. The symptoms of BPSD in AD are
very important to recognize and treat as they often pose the
greatest challenge to the caregivers and the health providers and
can be the direct cause of institutionalization of the patients. The
newer antidepressants and neuroleptics are the mainstay of medical
treatment and the treatment is often effective. Caution and close
monitoring of effects and side effects is warranted.
Acetylcholine deficit has been shown to be closely linked to the
cognitive decline in AD. A significant progress in the management
of the disease followed by the introduction of the Cholinesterase
inhibitors. These drugs have now gained a wide acceptance as the
cornerstone of medical treatment during the mild to moderate
stages of the disease even though their overall effect is modest at
best. Although the three drugs currently on the market all act by
inhibiting the function of the acetylcholine degrading enzyme
(AchE), they have different profile of action which will be dis-
cussed in more detail.
Other possible options of today's treatment are Ginkgo biloba,
vitamin-E, estrogens, statins and NSAIDs. None of these have been
established yet as being effective for the treatment of Alzheimer's
disease.
Many new drugs directly aimed at AD are currently in the pipe-
lines within the pharmaceutical industry. Some of them are acting
on the cholinergic system as muscarinic or nicotinic agonists. Others
are aiming towards more fundamental pathology such as the (}- or
y-secretase inhibitors. Yet another mode of action is promoting the
release of nerve growth factors. The mechanisms of several of these
potential future drugs will be discussed in more detail.
L54 - Sporadic vascular dementia subtypes - an update
Anders Wallin
Institute of Clinical Neuroscience, Sahlgrenska University Hospital/Mölndal,
Sweden
Sporadic vascular dementia, now judged to be the second most
common type of dementia, accounts for 10-50% of all dementia
cases. It has become clear that vascular disease is a risk factor for
cognitive impairment and dementia, not only vascular dementia but
also AD. With the variation in prevalence figures, diagnostic
criteria and pathophysiological mechanisms, vascular dementia
must be considered a heterogeneous concept.
In subcortical vascular dementia, the primary types of brain
lesions are lacunar infarcts and ischaemic white matter lesions, with
demyelination and loss of axons, a decreased number of oligo-
dendrocytes, reactive astrocytosis, and the primary lesion site is the
subcortical region. Changes in the levels of structural proteins in
the cerebrospinal fluid (CSF) may reflect pathophysiological mec-
hanisms and may also serve as markers in the clinical differentiation
between subcortical vascular dementia and “pure” Alzheimer's
disease. Potential CSF biochemical markers for subcortical vascular
dementia include the CSF/serum albumin ratio (for identification
of blood-brain barrier damage related to disturbances in the small
intracerebral vessels), CSF sulfatide (for identification of demyeli-
nation related to white-matter changes, CSF tau and CSF neurofila-
ment light protein (NFL) (for identification of axonal degenera-
tion), and CSF b amyloid protein (for identification of amyloid
mismetabolism).
Subcortical vascular dementia fulfils what can be referred to as
the basic criteria for a disease: the presence of a distinct pattern of
clinical features, i.e., subcortical (or frontosubcortical) symptoms,
that matches a distinct pathological picture. The opposite seems to
be true in post-stroke dementia, which has symptomatological
variation and relatively heterogeneous aetiology, i.e., thromboem-
bolism or haemorrhage. AD + vascular dementia is also hetero-
geneous with regard to both clinical picture and (by definition)
aetiology.
The large clinicopathological spectrum of ‘arteriosclerotic de-
mentia’ has again become a focus of attention. There is as yet no
approved pharmacological treatment for vascular dementia, but
risk factor management may be beneficial. It seems clear that
harmonisation of the criteria for vascular dementia and its subtypes
would facilitate research in this field. International acceptance of
the currently suggested criteria for subcortical vascular dementia
would provide a good starting-point for comparisons of treatment
responses across studies worldwide.
L55 - Genealogic approach to neurological diseases
Stefánsson K
deCODE genetics, Reykjavík, Iceland
Abstract not received.
L56 - Epidemiology And Genetics Of Parkinson's Disease In
lceland
Sveinbjörnsdóttir S
Dept. of Neurology, Landspítali University Hospital Grensás, Reykjavík, Iceland
Abstract not received.
L58 - Localization of a susceptibility gene for common forms of
stroke
Gretarsdottir S', Sveinbjörnsdottir Sz, Jonsson HH', Jakobsson P,
Einarsdottir E', Agnarsson U3, Skholny D', Einarsson G2, Gudjonsdottir
HM', Valdimarsson EM2, Einarsson ÓB’, Thorgeirsson G3, Hadzic R',
Jonsdottir S', Reynisdottir ST', Bjarnadottir SM', Gudmundsdottir Þ',
Gudlaugsdottir GJ3, Gill R4, Lindpaintner K4, Sainz J', Hannesson H',
Sigurdsson GT’, Frigge ML', Kong A', Gudnason V3, Stefansson K',
Gulcher JR'
'deCODE genetics, Sturlugata 8, IS 101-Reykjavik, Iceland, 2National University
Hospital, IS 101-Reykjavik, Iceland, ’lcelandic Heart Association Heart Preventive
Clinic, 108-Reykjavik, Iceland, 4F. Hoffmann La Roche, Grenzacher strasse, CH-
4070 Basel, Switzerland
Stroke is one of the most complex diseases of man with several
subtypes as well as secondary risk factors such as hypertension,
hyperlipidemia, and diabetes, which in turn have genetic and
environmental risk factors of their own.
We have mapped the first major locus for common forms of
stroke. In our study we used a broad but rigorous definition of the
stroke phenotype including hemorrhagic stroke, ischemic stroke
and transient ischemic attack. We cross-matched a population-
based list of stroke patients in Iceland with an extensive compu-
terized genealogy database clustering 476 stroke patients within 179
34 Læknablaðið/Fylgirít 43 2002/88