The Brain Disease of Ageing — Epidemiology and Risk Factors of Senile Dementia (Alzheimer)

1990 ◽  
pp. 2-17 ◽  
Author(s):  
H. Häfner
Keyword(s):  
Risk Factors ◽  
Senile Dementia ◽  
Brain Disease ◽  
The Brain

scholarly journals Alzheimer and vascular brain disease: Senile dementia

2015 ◽  
Vol 9 (2) ◽  
pp. 184-188 ◽  
Author(s):  
Eliasz Engelhardt ◽  
Lea T. Grinberg
Keyword(s):  
Senile Dementia ◽  
Vascular Cognitive Impairment ◽  
Brain Disease ◽  
Brain Diseases ◽  
Heterogeneous Condition ◽  
Disease Subtype ◽  
Wide Range ◽  
Alois Alzheimer ◽  
Short Time ◽  
The Brain

Alois Alzheimer is best known for his description of a novel disease, subsequently named after him. However, his wide range of interests also included vascular brain diseases. He described Senile dementia, a highly heterogeneous condition, and was able not only to distinguish it from syphilitic brain disease, but also to discriminate two clinicopathological subtypes, that may be labeled a "arteriosclerotic subtype", comparable to the present clinicopathological continuum of "Vascular cognitive impairment", and another as a "neurodegenerative subtype", characterized by primary [cortical] ganglion cell [nerve cells] degeneration, possibly foreshadowing a peculiar presenile disease that he was to describe some years later and would carry his name. He also considered the possibility of a senile presentation of this disease subtype, which was described by Oskar Fischer a short time later. Considering the clinicopathological overlapping features of the "arteriosclerotic subtype" of Senile dementia with Arteriosclerotic atrophy of the brain, it might be possible to consider that both represent a single condition.

scholarly journals A cybernetic perspective on the nature of psychopathology: Transcending conceptions of mental illness as statistical deviance and brain disease

2021 ◽  
Author(s):  
Colin G. DeYoung ◽  
Robert Krueger
Keyword(s):  
Risk Factors ◽  
Mental Illness ◽  
Brain Disease ◽  
Psychiatric Research ◽  
Neural Function ◽  
Personality Theory ◽  
Prevention And Treatment ◽  
Novel Theory ◽  
The Brain ◽  
Dominant Paradigm

Explicitly or implicitly, psychopathology is often defined in terms of statistical deviance, requiring that an affected individual is sufficiently distant from the norm in some dimension of psychological or neural function. In recent decades, the dominant paradigm in psychiatric research has focused primarily on deviance in neural function, treating psychopathology as disease of the brain. We argue that these conceptualizations are misguided. We recently proposed a novel theory of psychopathology, based in cybernetics and drawing additionally from neuroscience, psychometrics, and personality theory (DeYoung & Krueger, 2018a). In this theory, deviations from the norm in psychological and neural functioning serve as important risk factors for psychopathology but are not in themselves necessary or sufficient to identify psychopathology, which requires the presence of cybernetic dysfunction. Psychopathology is defined as persistent failure to move toward one’s goals, due to failure to generate effective new goals, interpretations, or strategies when existing ones prove unsuccessful. We argue that adopting a cybernetic theory to replace conceptualizations of psychopathology as statistical deviance or brain disease would facilitate improvements in measurement, diagnosis, prevention, and treatment of psychopathology.

CLINICAL AND NEUROLOGICAL FEATURES OF TRAUMATIC BRAIN DISEASE DURING THE STAGES OF REHABILITATION

2020 ◽  
Vol 3 (1) ◽  
pp. 51-53
Author(s):  
Rano Azizova ◽  
◽  
Umida Shamsiyeva ◽  
Mirzohid Turabbayev ◽  
Begzod Jorayev ◽  
...  
Keyword(s):  
Mechanical Energy ◽  
Pathological Process ◽  
Brain Disease ◽  
Clinical Forms ◽  
Neurological Features ◽  
Mechanisms Of Development ◽  
The Brain

Traumatic brain disease (TBHD) is a pathological process triggered by the damaging effect of mechanical energy on the brain and is characterized — with a variety of clinical forms — by the unity of etiology, pathogenetic and sanogenetic mechanisms of development and outcomes.

scholarly journals Addiction as a brain disease revised: why it still matters, and the need for consilience

2021 ◽  
Author(s):  
Markus Heilig ◽  
James MacKillop ◽  
Diana Martinez ◽  
Jürgen Rehm ◽  
Lorenzo Leggio ◽  
...  
Keyword(s):  
Spontaneous Remission ◽  
Brain Disease ◽  
Substance Addiction ◽  
Alternative Reinforcement ◽  
Sociocultural Perspectives ◽  
Compulsive Behaviors ◽  
Biological Substrate ◽  
Neural Signature ◽  
The Brain ◽  
Neuroscience Community

AbstractThe view that substance addiction is a brain disease, although widely accepted in the neuroscience community, has become subject to acerbic criticism in recent years. These criticisms state that the brain disease view is deterministic, fails to account for heterogeneity in remission and recovery, places too much emphasis on a compulsive dimension of addiction, and that a specific neural signature of addiction has not been identified. We acknowledge that some of these criticisms have merit, but assert that the foundational premise that addiction has a neurobiological basis is fundamentally sound. We also emphasize that denying that addiction is a brain disease is a harmful standpoint since it contributes to reducing access to healthcare and treatment, the consequences of which are catastrophic. Here, we therefore address these criticisms, and in doing so provide a contemporary update of the brain disease view of addiction. We provide arguments to support this view, discuss why apparently spontaneous remission does not negate it, and how seemingly compulsive behaviors can co-exist with the sensitivity to alternative reinforcement in addiction. Most importantly, we argue that the brain is the biological substrate from which both addiction and the capacity for behavior change arise, arguing for an intensified neuroscientific study of recovery. More broadly, we propose that these disagreements reveal the need for multidisciplinary research that integrates neuroscientific, behavioral, clinical, and sociocultural perspectives.

scholarly journals Changes in the Brain-Derived Neurotrophic Factor Are Associated with Improvements in Diabetes Risk Factors after Exercise Training in Adolescents with Obesity: The HEARTY Randomized Controlled Trial

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Jeremy J. Walsh ◽  
Amedeo D’Angiulli ◽  
Jameason D. Cameron ◽  
Ronald J. Sigal ◽  
Glen P. Kenny ◽  
...  
Keyword(s):  
Risk Factors ◽  
Exercise Training ◽  
Neurotrophic Factor ◽  
Fasting Glucose ◽  
Brain Derived Neurotrophic Factor ◽  
Diabetes Risk ◽  
Model Assessment ◽  
Neurocognitive Deficits ◽  
Diabetes Risk Factors ◽  
The Brain

Obesity in youth increases the risk of type 2 diabetes (T2D), and both are risk factors for neurocognitive deficits. Exercise attenuates the risk of obesity and T2D while improving cognitive function. In adults, these benefits are associated with the actions of the brain-derived neurotrophic factor (BDNF), a protein critical in modulating neuroplasticity, glucose regulation, fat oxidation, and appetite regulation in adults. However, little research exists in youth. This study examined the associations between changes in diabetes risk factors and changes in BDNF levels after 6 months of exercise training in adolescents with obesity. The sample consisted of 202 postpubertal adolescents with obesity (70% females) aged 14–18 years who were randomized to 6 months of aerobic and/or resistance training or nonexercise control. All participants received a healthy eating plan designed to induce a 250/kcal deficit per day. Resting serum BDNF levels and diabetes risk factors, such as fasting glucose, insulin, homeostasis model assessment (HOMA-B—beta cell insulin secretory capacity) and (HOMA-IS—insulin sensitivity), and hemoglobin A1c (HbA1c), were measured after an overnight fast at baseline and 6 months. There were no significant intergroup differences on changes in BDNF or diabetes risk factors. In the exercise group, increases in BDNF were associated with reductions in fasting glucose (β = −6.57, SE = 3.37, p=0.05) and increases in HOMA-B (β = 0.093, SE = 0.03, p=0.004) after controlling for confounders. No associations were found between changes in diabetes risk factors and BDNF in controls. In conclusion, exercise-induced reductions in some diabetes risk factors were associated with increases in BDNF in adolescents with obesity, suggesting that exercise training may be an effective strategy to promote metabolic health and increases in BDNF, a protein favoring neuroplasticity. This trial is registered with ClinicalTrials.gov NCT00195858, September 12, 2005 (funded by the Canadian Institutes of Health Research).

In vivo exploration of brain phosphorus 31 metabolism in patients with senile dementia of Alzheimer type

1994 ◽  
Vol 9 (2) ◽  
pp. 105-109
Author(s):  
G Mecheri ◽  
Y Bissuel ◽  
J Dalery ◽  
JL Terra ◽  
G Balvay ◽  
...  
Keyword(s):  
Statistical Analysis ◽  
Senile Dementia ◽  
Phospholipid Metabolism ◽  
Alzheimer Type ◽  
Dementia Of Alzheimer Type ◽  
Non Invasive ◽  
Significant Difference ◽  
The Brain

SummaryIn vivo NMR 31p spectroscopy is a non invasive, non ionizing method of exploration of energy and phospholipid metabolism in the brain. This study consisted of comparing 31p spectra in five patients with Senile Dementia of Alzheimer Type (SDAT) with those of four controls of similar ages. Abnormal phosphonionocsters (PME) concentrations, either high or low, were found in the patients, but statistical analysis did not elicit any significant difference relative to controls.

Brain Injury in a Healthy Child One Year After Periureteral Injection of Teflon

PEDIATRICS ◽  
1996 ◽  
Vol 98 (2) ◽  
pp. 290-291
Author(s):  
Renato Borgatti ◽  
Alberto Tettamanti ◽  
Paolo Piccinelli
Keyword(s):  
Risk Factors ◽  
Brain Injury ◽  
Middle Cerebral Artery ◽  
Vesicoureteral Reflux ◽  
Healthy Child ◽  
Endoscopic Injection ◽  
Middle Cerebral Artery Stroke ◽  
One Year ◽  
Lateral Branches ◽  
The Brain

This report presents the case of a previously healthy 6-year-old girl who had an ischemic injury corresponding to the territory perfused by the lateral branches of the lenticulostriate arteries of the middle cerebral artery. Stroke in childhood is rare, and the specific causes are identified in only half the cases. Our patient was carefully studied for any hereditary or acqired risk Factors for stroke, but we found only one, an endoscopic injection of Teflon performed 1 year before to correct vesicoureteral reflux. This suggests the risk of potential migration of Teflon particles to the brain, here they can block the microcirculation.

scholarly journals Association between Risk Factors for Vascular Dementia and Adiponectin

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
Juhyun Song ◽  
Won Taek Lee ◽  
Kyung Ah Park ◽  
Jong Eun Lee
Keyword(s):  
Risk Factors ◽  
Cardiovascular Disease ◽  
Signal Transduction ◽  
Vascular Dementia ◽  
Case Control ◽  
Case Control Studies ◽  
Insulin Signal Transduction ◽  
Increased Risk ◽  
The Brain

Vascular dementia is caused by various factors, including increased age, diabetes, hypertension, atherosclerosis, and stroke. Adiponectin is an adipokine secreted by adipose tissue. Adiponectin is widely known as a regulating factor related to cardiovascular disease and diabetes. Adiponectin plasma levels decrease with age. Decreased adiponectin increases the risk of cardiovascular disease and diabetes. Adiponectin improves hypertension and atherosclerosis by acting as a vasodilator and antiatherogenic factor. Moreover, adiponectin is involved in cognitive dysfunction via modulation of insulin signal transduction in the brain. Case-control studies demonstrate the association between low adiponectin and increased risk of stroke, hypertension, and diabetes. This review summarizes the recent findings on the association between risk factors for vascular dementia and adiponectin. To emphasize this relationship, we will discuss the importance of research regarding the role of adiponectin in vascular dementia.

Sign in / Sign up

Export Citation Format

Share Document