Mental-behavioral disorders in Alzheimer's disease

Behavioural and psychological disorders are often observed in Alzheimer's disease. Some are common, such as symptoms of depression, apathy, aggressivity, agitation, psychotic disturbances, disorders of sleep rhythm, etc. Many factors contribute to the aetiology of these disorders, mainly cerebral lesions, environmental changes, somatic illnesses, iatrogenic factors and psychological reaction mechanisms. Management must take each into account. Treatment comprises medication (symptomatic treatment of the various disorders, cholinergic treatment) and other means (adaptation of the inhabitation, informing family and friends, psychotherapy, etc.).     

Circadian rhythm disorders, motivation and Alzheimer's disease

In Alzheimer's disease, when the breakdown of the sleep's circadian rythm is sudden, it reflects frequently a concomitant somatic or psychiatric disorder. If the trouble appears progressively, there is less pathological or disturbing behaviors in the beginning. Later, it is often associated with a loss of interest for the daily living activities (perte de motivation).     

Neurological disorders in dentistry: managing patients with Alzheimer's disease

Alzheimer's disease (AD) is the most prevalent type of dementing illness affecting over four million Americans. It typically occurs after age 60, and prevalence increases with advanced age. As the adult population increases, a greater number of patients with a diagnosis of AD will require dental care. This article reviews the oral and systemic clinical findings seen in AD patients and current medical treatment. Some general and specific suggestions for dental management are presented, including guidelines for restraint and sedation use. Finally, some helpful, adaptive oral devices are recommended for use by caregivers of patients unable to provide for their own daily oral hygiene. Dental providers can and should be willing to make oral care available to patients with a diagnosis of AD. Despite the difficulties involved, the need will continue to be great, and the gratification in caring for these patients makes it worth the effort.     

Oxidative alterations in Alzheimer's disease

The expression of heparin-binding epidermal growth factor-like growth factor (HB-EGF), an EGF receptor ligand, was investigated in rat forebrain under basal conditions and after kainate-induced excitotoxic seizures. In addition, a potential neuroprotective role for HB-EGF was assessed in hippocampal cultures. In situ hybridization analysis of HB-EGF mRNA in developing rat hippocampus revealed its expression in all principle cell layers of hippocampus from birth to postnatal day (P) 7, whereas from P14 through adulthood, expression decreased in the pyramidal cell layer versus the dentate gyrus granule cells. After kainate-induced excitotoxic seizures, levels of HB-EGF mRNA increased markedly in the hippocampus, as well as in several other cortical and limbic forebrain regions. In the hippocampus, HB-EGF mRNA expression increased within 3 hr after kainate treatment, continued to increase until 24 hr, and then decreased; increases occurred in the dentate gyrus granule cells, in the molecular layer of the dentate gyrus, and in and around hippocampal pyramidal CA3 and CA1 neurons. At 48 hr after kainate treatment, HB-EGF mRNA remained elevated in vulnerable brain regions of the hippocampus and amygdaloid complex. Western blot analysis revealed increased levels of HB-EGF protein in the hippocampus after kainate administration, with a peak at 24 hr. Pretreatment of embryonic hippocampal cell cultures with HB-EGF protected neurons against kainate toxicity. The kainate-induced elevation of [Ca2+]i in hippocampal neurons was not altered in cultures pretreated with HB-EGF, suggesting an excitoprotective mechanism different from that of previously characterized excitoprotective growth factors. Taken together, these results suggest that HB-EGF may function as an endogenous neuroprotective agent after seizure-induced neural activity/injury.     

Convergence of Lewy bodies and neurofibrillary tangles in amygdala neurons of Alzheimer's disease and Lewy body disorders

Amygdalae of patients with Alzheimer's disease (AD), Parkinson's disease, Down's syndrome, diffuse Lewy body disease or a combination of these diseases were probed with antibodies to neurofilament proteins as well as with Lewy body (LB)- and paired helical filament-specific antibodies. The results indicate that the amygdala is severely affected by the accumulation of both neurofibrillary tangles (NFTs) and LBs in most cases of the diseases mentioned above, and that amygdala LBs have a similar epitope composition to that of LBs in the brain stem and cerebral cortex. While large numbers of both LBs and NFTs were seen in different neurons within the amygdala, these two lesions frequently occurred together in the same neurons of the amygdala. These findings are in contrast to other sites that accumulate LBs and NFTs, but rarely both lesions in the same neuron. Thus, amygdala neurons may be selectively vulnerable to developing both LBs and NFTs, and these inclusions may play a role in the massive degeneration of these neurons in AD and LB disorders of the elderly.     

The cholinergic system in Alzheimer's disease

The past decade has witnessed an enormous increase in our knowledge of the variety and complexity of neuropathological and neurochemical changes in Alzheimer's disease. Although the disease is characterized by multiple deficits of neurotransmitters in the brain, this overview emphasizes the structural and neurochemical localization of the elements of the acetylcholine system (choline acetyltransferase, acetylcholinesterase, and muscarinic and nicotinic acetylcholine receptors) in the non-demented brain and in Alzheimer's disease brain samples. The results demonstrate a great variation in the distribution of acetylcholinesterase, choline acetyltransferase, and the nicotinic and muscarinic acetylcholine receptors in the different brain areas, nuclei and subnuclei. When stratification is present in certain brain regions (olfactory bulb, cortex, hippocampus, etc.), differences can be detected as regards the laminar distribution of the elements of the acetylcholine system. Alzheimer's disease involves a substantial loss of the elements of the cholinergic system. There is evidence that the most affected areas include the cortex, the entorhinal area, the hippocampus, the ventral striatum and the basal part of the forebrain. Other brain areas are less affected. The fact that the acetylcholine system, which plays a significant role in the memory function, is seriously impaired in Alzheimer's disease has accelerated work on the development of new drugs for treatment of the disease of the 20th century.     

Contrast sensitivity dysfunction in Alzheimer's disease

We compared the spatial contrast sensitivity of six patients with mild to moderate Alzheimer's disease (AD) and six age-matched control subjects in a parametric design. Results demonstrate reduced contrast sensitivity in patients with AD at all but the lowest frequency tested. The results suggest that the effect of AD on spatial contrast sensitivity is stronger at higher frequencies and provide a rationale for complaints of poor vision in AD patients.     

Behavior and affect in Alzheimer's disease

The behavioral symptoms associated with AD are a critical aspect of the disease. They provide an additional avenue not only for understanding AD but for implementing interventions. The nature of behavioral disorders in AD is complicated by a number of factors that interact and contribute to the development of problematic behavior. It is difficult to determine whether the behavior is the result of neurodegeneration, cognitive dysfunction, previous experiences, current stressors, independently coexisting psychopathology, or a combination of these factors. In any case, behavioral disturbances need to be more clearly defined and objectively measured. To understand and treat behavioral disturbances in AD, all biopsy-chosocial factors must be examined simultaneously. Currently, there is little that can be done to treat the cognitive components of AD. Consequently, our most successful and beneficial interventions may focus on the remediable behavioral manifestations of the disease. The most valuable treatment approach for patients with AD and their caregivers interweaves medications, psychosocial services, environmental strategies, and caregiver education.     

Interhemispheric disconnection syndrome in Alzheimer's disease

It is commonly acknowledged that patients with Alzheimer's disease show memory and cognitive deficits that result from their cerebral histopathological abnormalities. We report new evidence showing that they also manifest deficits in interhemispheric integration of information, probably reflecting a corpus callosum dysfunction. Patients were given a battery of motor, somatosensory, and visual tests that had to be carried out by using either one or both hemispheres. Tasks were chosen such that subjects with Alzheimer's disease performed normally when using intrahemispheric processing. They, however, performed poorly when interhemispheric communication was required. This observation attests to the presence of a disconnection syndrome and suggests that these interhemispheric tasks can serve as diagnostic tools for the early assessment of their dementia.