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Biomedical subjects

J T Becker

Publications and source records attributed to J T Becker.

115 records · Page 7Linked to original sources
PubMedDate not supplied

A positron emission tomography (PET) study of autobiographical memory retrieval.

Memory for the experiences of one's life, autobiographical memory (AM), is one of the most human types of memory, yet comparatively little is known of its neurobiology. A positron emission tomography (PET) study of AM retrieval revealed that the left frontal cortex was significantly active during retrieval (compared to memory control tasks), together with activation in the inferior temporal and occipital lobes in the left hemisphere. We propose that this left frontal lobe activation reflects the operation of control processes that modulate the construction of AMs in posterior neocortical networks.

Adult↗
PubMedDate not supplied

Dementia accompanying motor neuron disease.

This study presents a structural and clinical description of a patient with dementia of motor neuron disease (D-MND), and compares and contrasts the neuropsychological characteristics of this patient with those of a group of patients with Alzheimer's disease (AD) matched by severity of dementia. The D-MND patient as well as the AD patients performed abnormally on all tasks that assessed executive/frontal functions. However, the D-MND patient tended to be more impaired than AD patients on tasks that required high speed decisions and on shifting from one strategy to another. Deficits in memory, language, and lexical-semantic abilities were also apparent in this patient. The co-occurrence of signs and symptoms characteristics of 'subcortical' dementia with those of 'cortical' dementia suggest that the executive system dysfunction may be secondary to subcortical pathology.

Alzheimer Disease↗
PubMedDate not supplied

Electroencephalographic correlates of periventricular white matter lesions in probable Alzheimer's disease.

We evaluated the relationship between periventricular white matter lesions (PWMLs) and EEG abnormalities in probable Alzheimer's disease (AD). We visually analyzed the EEG of 27 probable AD patients with mild to moderate degree of cognitive impairment participating in a longitudinal study of dementia. Patients had both CT and MRI scans performed at baseline examination, which also included an EEG. PWMLs were rated in CT and MRI films using a semiquantitative method. The EEGs were classified according to the Mayo Clinic Classification System. Abnormal EEGs correlated with PWMLs rating scores were detected on CT, but not on MRI. These data suggest that the presence of PWMLs contribute to the abnormal EEGs observed in AD patients, and that white matter abnormalities in CT correlate better with both the clinical findings and EEG than does the more sensitive but less specific MRI.

Aged↗
PubMedDate not supplied

[The semantic memory deficit in Alzheimer's disease].

INTRODUCTION AND DEVELOPMENT: Although the loss of episodic memory is considered one of the the hallmarks of Alzheimer s disease (AD), it is by no means the only memory dysfunction suffered by these patients. Perhaps equally important in terms of functional adaptation is the loss of, what Tulving referred, semantic memory. Semantic memory is that information necessary for language, a mental diccionary including not only lexical information (i.e., word meaning and concepts) but also facts and general world knowledge. There is a debate in the field of cognitive psychology regarding semantic memory, deficits in AD; whether there is an actual defect in semantic memory, or this is related to a disruption of the information accessing process. Neuroimaging studies have shown that the basis of the semantic memory defect is localized in the temporal and frontal lobes. CONCLUSIONS: The inferior temporal lobe, and perhaps more importantly, the parahippocampal gyrus, is critical for the ability to successfully name objects. However, the ability to retrieve name of objects appears to be associated with the frontal lobes.

Alzheimer Disease↗
PubMedDate not supplied

[Treatment of Alzheimer's disease].

OBJECTIVE: To review the experience of the last twenty years in the treatment of Alzheimer s disease (AD). METHODS: Literature review. RESULTS: The neuropathological bases of AD are centered on two important pathophysiological mechanisms: 1) Structural damage (e.g., senile plaques, neurofibrillary tangles, neuronal loss, inflammatory processes), and 2) Loss of cholinergic neurons (and acetylcholine depletion) in the nucleus basalis of Meynert, which sends cholinergic projections to all areas of the neocortex, especially the temporal lobes and frontal and parietal association areas. The indemnity of this system is essential for normal cognitive functioning. At this moment, the only long term treatment available for AD are acetylcholinesterase inhibitors (CEIs) (e.g., tacrine, donepezil, rivastigmine, galanthamine). There are being investigated several treatments that may alter the development of neurofibrillary tangles and neuritic plaques (e.g., peripherally administered antibodies against beta amyloid proteins). Nerve growth factors may have the capability of improving neuronal survival, although their form of administration remains a problem. Amelioration of oxidative stress and CNS inflammatory processes may slow dawn the rate of neurodegeneration. CONCLUSION: All suspected mechanisms of the metabolic cascade of AD have been explored with specific and non specific treatments. Current treatments (e.g., CEIs) still have to prove that their effects can last for long periods of time. With the advent of further understanding of the neurodegenerative processes that cause AD, new treatments that may slow down the progression of the disease will be available.

Acetylcholine↗
PubMedDate not supplied

[Factors that modify the natural course of Alzheimer's disease].

Alzheimer s disease (AD) is an insidious, and progressive disorder of the nervous system that typically occurs after age 65, with incidence rising with chronological age. The disorder is characterized by a pronounced memory loss, due to neuropathological changes in the mesial temporal lobes; as the pathology spreads throughout the cerebral cortex. However, it is still unknown why some areas are more affected than others, with the subsequent clinical heterogeneity (or phenotypes), and variability in the clinical course. The most salient neurobehavioral syndromes that can affect the clinical course are extrapyramidal signs, as well as a wide variety of psychiatric syndromes (e.g., psychotic symptoms, depression, aggression). Similarly, medication use (e.g., antipsychotics, sedatives) have shown to have a detrimental effect in the course of the disease. Current palliative treatments for AD may alter the natural history of the disease by extending the time that affected patients may live at home.

Alcoholism↗