Somatostatin-Positive Neurons in the Different Parts of the Brain in Normal Aging and Alzheimer's Disease

Neurosignals ◽  
1996 ◽  
Vol 5 (6) ◽  
pp. 343-348 ◽  
Author(s):  
Wei Ping Li ◽  
Helen W.L. Lai ◽  
Suet Ying Cheng ◽  
David T. Yew
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Normal Aging ◽  
The Brain ◽  
Different Parts

Differences in EEG Harmonic Driving Responses to Photic Stimulation between Normal Aging and Alzheimer's Disease

2002 ◽  
Vol 33 (2) ◽  
pp. 86-92 ◽  
Author(s):  
Mitsuru Kikuchi ◽  
Yuji Wada ◽  
Yoshifumi Koshino
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Functional Organization ◽  
Brain Activation ◽  
The Elderly ◽  
Normal Aging ◽  
Photic Stimulation ◽  
Elderly Subjects ◽  
Absolute Power ◽  
The Brain

In order to investigate whether Alzheimer's disease (AD) is the end result of aging of the brain or the result of some other mechanism, we analyzed EEGs showing the absolute power of harmonic responses to photic stimulation (PS) in younger subjects, non-demented elderly subjects and AD patients. At rest, the AD patients generally showed less absolute power than the younger and elderly subjects, with significant differences found at 10Hz and 20Hz. Analysis of EEGs recorded during PS indicated that the elderly subjects generally demonstrated more absolute power than the younger subjects and AD patients. These findings suggest a failure of stimulation-related brain activation in AD patients, and provide further evidence that normal aging and AD employ different mechanisms for functional organization during PS.

Understanding the role of histone deacetylase and their inhibitors in neurodegenerative disorders: Current targets and future perspective

2021 ◽  
Vol 19 ◽  
Author(s):  
Vishal Kumar ◽  
Satyabrata Kundu ◽  
Arti Singh ◽  
Shamsher Singh
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Spinal Cord ◽  
Histone Deacetylase ◽  
Neurodegenerative Disorders ◽  
Future Perspective ◽  
Class Iii ◽  
Pathological Conditions ◽  
The Brain ◽  
Different Parts

: Neurodegenerative diseases are the group of pathological conditions that cause motor inc-ordination (jerking movements), cognitive and memory impairments result due to degeneration of neurons in a specific area of the brain. Oxidative stress, mitochondrial dysfunction, excitotoxicity, neuroinflammation, neurochemical imbalance and histone deacetylase enzymes (HDAC) are known to play a crucial role in neurodegeneration. HDAC is classified into four categories (class I, II, III and class IV) depending upon their location and functions. HDAC1 and 2 are involved in neurodegeneration while HDAC3-11 and class III HDACs are beneficial as neuroprotective. HDACs are localized in different parts of the brain- HDAC1 (hippocampus and cortex), HDAC2 (nucleus), HDAC3, 4, 5, 7 and 9 (nucleus and cytoplasm), HDAC6 & HDAC7 (cytoplasm) and HDAC11 (Nucleus, Cornus ammonis 1 and spinal cord). In pathological conditions, HDAC up-regulates glutamate, phosphorylation of tau, and glial fibrillary acidic proteins while down-regulates BDNF, Heat shock protein 70, Gelsolin. Class III HDACs are divided into seven sub-classes (SIRT1-SIRT7). Sirtuins are localized in the different parts of the brain and neuron -Sirt1 (nucleus), Sirt2 (cortex, striatum, hippocampus and spinal cord), Sirt3 (mitochondria and cytoplasm), Sirt4, Sirt5 & Sirt6 (mitochondria), Sirt7 (nucleus) and Sirt8 (nucleolus). SIRTs (1, 3, 4, and 6) are involved in neuronal survival, proliferation and modulating stress response, and SIRT2 is associated with Parkinsonism, Huntington disease and Alzheimer’s disease, whereas, SIRT6 is only associated with Alzheimer’s disease. In this critical review, we have discussed the mechanisms and therapeutic targets of HDACs would be beneficial for the management of neurodegenerative disorders.

Longitudinal Changes in Individual BrainAGE in Healthy Aging, Mild Cognitive Impairment, and Alzheimer’s Disease

GeroPsych ◽  
2012 ◽  
Vol 25 (4) ◽  
pp. 235-245 ◽  
Author(s):  
Katja Franke ◽  
Christian Gaser
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Healthy Aging ◽  
Brain Aging ◽  
Elderly Subjects ◽  
Additional Increase ◽  
Longitudinal Changes ◽  
Novel Method ◽  
The Brain

We recently proposed a novel method that aggregates the multidimensional aging pattern across the brain to a single value. This method proved to provide stable and reliable estimates of brain aging – even across different scanners. While investigating longitudinal changes in BrainAGE in about 400 elderly subjects, we discovered that patients with Alzheimer’s disease and subjects who had converted to AD within 3 years showed accelerated brain atrophy by +6 years at baseline. An additional increase in BrainAGE accumulated to a score of about +9 years during follow-up. Accelerated brain aging was related to prospective cognitive decline and disease severity. In conclusion, the BrainAGE framework indicates discrepancies in brain aging and could thus serve as an indicator for cognitive functioning in the future.

The Weak Combined Magnetic Fields Reduce the Brain β-Amyloid in an Animal Model of Sporadic Alzheimer's Disease

PIERS Online ◽  
2009 ◽  
Vol 5 (4) ◽  
pp. 311-315 ◽  
Author(s):  
Natalia V. Bobkova ◽  
Vadim V. Novikov ◽  
Natalia I. Medvinskaya ◽  
Irina Yu. Aleksandrova ◽  
Eugenii E. Fesenko
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Animal Model ◽  
Magnetic Fields ◽  
Sporadic Alzheimer’S Disease ◽  
Combined Magnetic Fields ◽  
The Brain

SPECIFIC PROPERTIES OF TUBULIN IN THE PREFRONTAL CORTEX IN CONTROL, SCHIZOPHRENIA AND VASCULAR DEMENTIA

2020 ◽  
pp. 65-71
Author(s):  
Burbaeva G.Sh. ◽  
Androsova L.V. ◽  
Vorobyeva E.A. ◽  
Savushkina O.K.
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Prefrontal Cortex ◽  
Vascular Dementia ◽  
Binding Activity ◽  
Nephelometric Method ◽  
Rate Of Polymerization ◽  
Mental Diseases ◽  
And Control ◽  
The Brain

The aim of the study was to evaluate the rate of polymerization of tubulin into microtubules and determine the level of colchicine binding (colchicine-binding activity of tubulin) in the prefrontal cortex in schizophrenia, vascular dementia (VD) and control. Colchicine-binding activity of tubulin was determined by Sherlinе in tubulin-enriched extracts of proteins from the samples. Measurement of light scattering during the polymerization of the tubulin was carried out using the nephelometric method at a wavelength of 450-550 nm. There was a significant decrease in colchicine-binding activity and the rate of tubulin polymerization in the prefrontal cortex in both diseases, and in VD to a greater extent than in schizophrenia. The obtained results suggest that not only in Alzheimer's disease, but also in other mental diseases such as schizophrenia and VD, there is a decrease in the level of tubulin in the prefrontal cortex of the brain, although to a lesser extent than in Alzheimer's disease, and consequently the amount of microtubules.

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