ABSTRACT
Cognitive decline is well known to be connected to diabetes in presence of repetitive hyper- as well as hypoglycemia. At the Memory Clinic at CSK, Kristianstad, we have observed over 40 patients with cognitive decline and diabetes type I and II. Cognitive dysfunction seems to affect both compliance and the glucose levels. In collaboration with the diabetes unit at the Medicine Clinic, CSK, guidelines have been developed to aid early discovery of cognitive decline and adapted interventions aiming for optimal independence at home and at work. The possibility of these individually adapted interventions aiding in slowing down the rate of complications as well as the secondary risk of dementia is under observation.
Subject(s)
Cognition Disorders/etiology , Diabetes Mellitus, Type 1/complications , Diabetes Mellitus, Type 2/complications , Aged , Cognition Disorders/diagnosis , Cognition Disorders/prevention & control , Dementia/prevention & control , Early Diagnosis , Female , Humans , Male , Middle Aged , Neuropsychological Tests , Outpatient Clinics, Hospital , Risk FactorsSubject(s)
Continuity of Patient Care , Dementia , Intellectual Disability , Dementia/complications , Dementia/diagnosis , Dementia/therapy , Hospital Units/organization & administration , Humans , Intellectual Disability/complications , Intellectual Disability/psychology , Intellectual Disability/therapy , Interdisciplinary Communication , Practice Guidelines as Topic , SwedenABSTRACT
The knowledge regarding putative inflammatory component(s) participating in Alzheimer's disease (AD) and vascular dementia (VAD) is scarce. Recently, we have demonstrated the presence of certain inflammatory cytokines in the cerebrospinal fluid (CSF) of demented patients. Although the initial event(s) triggering the neurodegenerative processes in AD versus VAD may be different and lead to different neuropathological changes, it may initiate a similar cascade of cytokine production in response to neuronal injury. The cytokines released in the central nervous system (CNS) may, in turn, act in a similar manner in both diseases, amplifying some pathological changes such as amyloidogenesis and white matter lesions or on the contrary acting as neuroprotective molecules. This review will focus on the intracerebral production of the pro- and anti-inflammatory cytokines interleukin IL-1beta, IL-1 receptor antagonist (IL-1ra), IL-6 and TNF-alpha in dementia, and their relation to gene polymorphism, to cerebral neuronal damage, apoptosis, and to clinical variables of dementia. Our results, which show for the first time strikingly increased CSF levels of TNF-alpha but not of TNF-beta, IL-1beta or IL-6 in AD and VAD, may form a conceptual framework for further studies of neuroprotective mechanisms in dementias.
