Estado nutricional e consumo alimentar de pacientes brasileiros em diferentes estágios da doença de alzheimer: um estudo transversal / Nutritional status and food intake of Brazilian patients at various stages of Alzheimer's disease: a cross-sectional study

A doença de Alzheimer (DA) é caracterizada por distúrbios que podem comprometer a nutrição do paciente e causar perda de peso e deficiências nutricionais durante a doença. O objetivo deste estudo foi avaliar o estado nutricional e o consumo alimentar de pacientes brasileiros com doença de Alzheimer em diferentes estágios da doença. A amostra foi composta por 30 indivíduos, com idade média de 77 anos, de ambos os sexos, com provável DA. Os indivíduos foram avaliados através de dados antropométricos, Mini Avaliação Nutricional (MAN), albumina sérica, Mini Exame do Estado Mental, e recordatório de 24 horas. Embora tenha sido encontrada uma diminuição no peso médio entre os estágios da doença (CDR1: 70,8±15,9 kg; CDR2: 61,4±15,7 kg; CDR3: 56,1± 8,4kg) conforme a progressão da doença, a diferença não foi significativa. Os parâmetros MAN e albumina sérica mostraram uma diminuição entre os estágios da doença (p = 0,042,p = 0,047, respectivamente), sendo que no estágio grave metade dos pacientes estava desnutrida e a outra metade em risco de desnutrição. De acordo com o índice de massa corporal, 23,3% dos pacientes estavam com sobrepeso. O valor nutricional da ingestão alimentar foi similar nos estágios de DA. Em conclusão, a maioria dos pacientes brasileiros com DA neste estudo apresentaram desnutrição, apesar de o consumo alimentar ter sido similar entre os estágios da doença, uma vez que não apresentou associação direta com a progressão da DA...

Alzheimer's disease (AD) is characterized by disorders that can impair the nutrition of the patient and lead to weight loss and nutritional deficits during the course of the disease. The aim of this study was to assess the nutritional status and food intake of Brazilian patients with Alzheimer's disease at 3 different stages of the disease. The sample consisted of 30 subjects of both genders, mean age 77 years, with probable AD. Subjects were assessed by collecting anthropometric data, the Mini Nutritional Assessment (MNA), serum albumin content, Mini Mental State Examination and 24-hour records of food and drink. Although a steady decrease in average weight was observed as the disease progressed (CDR1: 70.8±15.9 kg; CDR2: 61.4±15.7 kg; CDR3: 56.1± 8.4 kg), the differences were not significant. MNA and serum albumin both fell during the progression of the disease (p = 0.042; p = 0.047, respectively) and, at the severe stage, half the patients were found to be undernourished and the other half at risk of undernutrition. According to their body mass index, 23.3% of patients were overweight. The nutritional value of the food consumed was similar across the stages of AD. In conclusion, the majority of Brazilian patients with AD in this study exhibited cognitive decline and malnutrition. However, food intake was similar among the stages of the disease, thus having no direct association with the progression of AD...

On the participation of hippocampal PKC in acquisition, consolidation and reconsolidation of spatial memory.

Memory consolidation involves a sequence of temporally defined and highly regulated changes in the activation state of several signaling pathways that leads to the lasting storage of an initially labile trace. Despite appearances, consolidation does not make memories permanent. It is now known that upon retrieval well-consolidated memories can become again vulnerable to the action of amnesic agents and in order to persist must undergo a protein synthesis-dependent process named reconsolidation. Experiments with genetically modified animals suggest that some PKC isoforms are important for spatial memory and earlier studies indicate that several PKC substrates are activated following spatial learning. Nevertheless, none of the reports published so far analyzed pharmacologically the role played by PKC during spatial memory processing. Using the conventional PKC and PKCmu inhibitor 12-(2-cyanoethyl)-6,7,12,13-tetrahydro-13-methyl-5-oxo-5H-indolo[2,3-a]pyrrollo[3,4-c]carbazole (Gö6976) we found that the activity of these kinases is required in the CA1 region of the rat dorsal hippocampus for acquisition and consolidation of spatial memory in the Morris water maze learning task. Our results also show that when infused into dorsal CA1 after non-reinforced retrieval, Gö6976 produces a long-lasting amnesia that is independent of the strength of the memory trace, suggesting that post-retrieval activation of hippocampal PKC is essential for persistence of spatial memory.

The connection between the hippocampal and the striatal memory systems of the brain: a review of recent findings.

Two major memory systems have been recognized over the years (Squire, in Memory and Brain, 1987): the declarative memory system, which is under the control of the hippocampus and related temporal lobe structures, and the procedural or habit memory system, which is under the control of the striatum and its connections (Mishkin et al., in Neurobiology of Learning by G Lynch et al., 1984; Knowlton et al., Science 273:1399, 1996). Most if not all learning tasks studied in animals, however, involve either the performance or the suppression of movement. Animals acquire connections between environmental or discrete sensory cues (conditioned stimuli, CSs) and emotionally or otherwise significant stimuli (unconditioned stimuli, USs). As a result, they learn to perform or to inhibit the performance of certain motor responses to the CS which, when learned well, become what can only be called habits (Mishkin et al., 1984): to regularly walk or swim to a place or away from a place, or to inhibit one or several forms of movement. These responses can be viewed as conditioned responses (CRs) and may sometimes be very complex. This is of course also seen in humans: people learn how to play on a keyboard in response to a mental or written script and perform the piano or write a text; with practice, the performance improves and eventually reaches a high criterion and becomes a habit, performed almost if not completely without awareness. Commuting to school in a big city in the shortest possible time and eschewing the dangers is a complex learning that children acquire to the point of near-perfection. It is agreed that the rules that connect the perception of the CS and the expression of the CR change from their first association to those that take place when the task is mastered. Does this change of rules involve a switch from one memory system to another? Are different brain systems used the first time one plays a sonata or goes to school as compared with the 100th time? Here we will comment on: 1) reversal learning in the Morris water maze (MWM), in which the declarative or spatial component of a task is changed but the procedural component (to swim) persists and needs to be re-linked with a different set of spatial cues; and 2) a series of observations on an inhibitory avoidance task that indicate that the brain systems involved change with further learning.

AMPA/kainate and group-I metabotropic receptor antagonists infused into different brain areas impair memory formation of inhibitory avoidance in rats.

Several lines of evidence suggest that glutamate receptors are involved in memory processing. To examine the role of non-N-methyl-D-aspartate (non-NMDA) glutamate receptors on memory consolidation, rats were bilaterally implanted with cannulae aimed at the CA1 region of the dorsal hippocampus (CA1), entorhinal cortex (ENTO), posterior parietal cortex (PPC) or the basolateral nucleus of the amygdala (BLA), and trained in a one-trial step-down inhibitory avoidance task. At different times after training, the alpha-amino 3-hydroxy-5 methyl 4-isoxazole propionate (AMPA) receptor blocker, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) (1.0 microg/side), or the metabotropic type-I receptor antagonist, 2-amino-3-phosphonopropionic acid (AP3) (1.0 microg/side), were infused into the above-mentioned structures. CNQX produced retrograde amnesia when infused into BLA or CA1 0, 30, 90 or 180 min post-training but not at later times. AP3 blocked memory consolidation when administered into CA1 0, 30 or 180 min post-training, while in BLA, it was amnestic only when given 0 or 30 min after the training session. CNQX and AP3 had no effect on memory when administered into ENTO or PPC at any time. Our data suggest that the consolidation of the avoidance memory requires intact non-NMDA receptor function in the hippocampus and the basolateral nucleus of the amygdala, but not necessarily in the entorhinal and parietal cortex, for long periods after training.