Safety And Supportive Measures
Creating a safe and supportive environment can be very helpful.
Generally, the environment should be bright, cheerful, safe, stable, and designed to help with orientation. Some stimulation, such as a radio or television, is helpful, but excessive stimulation should be avoided.
Structure and routine help people with Alzheimer disease stay oriented and give them a sense of security and stability. Any change in surroundings, routines, or caregivers should be explained to people clearly and simply.
Following a daily routine for tasks such as bathing, eating, and sleeping helps people with Alzheimer disease remember. Following a regular routine at bedtime may help them sleep better.
Activities scheduled on a regular basis can help people feel independent and needed by focusing their attention on pleasurable or useful tasks. Such activities should include physical and mental activities. Activities should be broken down in small parts or simplified as the dementia worsens.
How To Survive In The Diseased Brain
Monolayer neuronal cultures produced from human iPSCs derived from sporadic or familial cases of AD display AD associated abnormalities such as higher levels of A peptide and phosphorylated tau , endoplasmic reticulum and oxidative stress, down regulation of synaptic proteins and increased apoptosis . These findings reveal that neurons derived from AD-specific iPSCs can reproduce AD traits spontaneously in vitro. Furthermore, the neurons differentiated from iPSCs produced from somatic cells obtained from familial cases of AD are more vulnerable when they are exposed to A aggregates in vitro .
Loss Of Two Types Of Neurons Triggers Parkinson’s Symptoms Study Suggests
- Emory University
- New evidence indicates that the loss of two types of brain cells — not just one as previously thought — may trigger the onset of symptoms associated with Parkinson’s disease. The evidence, based on mouse models, shows a link between the loss of both norepinephrine and dopamine neurons and the delayed onset of symptoms associated with Parkinson’s disease. It was originally thought that the loss of only dopamine neurons triggered symptoms. Dopamine is a neurotransmitter critical for coordinating movement.
New evidence indicates that the loss of two types of brain cells–not just one as previously thought–may trigger the onset of symptoms associated with Parkinson’s disease.
The evidence, based on mouse models, shows a link between the loss of both norepinephrine and dopamine neurons and the delayed onset of symptoms associated with Parkinson’s disease. It was originally thought that the loss of only dopamine neurons triggered symptoms. Dopamine is a neurotransmitter critical for coordinating movement.
The research was conducted by Karen Rommelfanger, graduate student in the laboratory of David Weinshenker, PhD, assistant professor of human genetics in Emory University School of Medicine and Gary Miller, PhD, associate professor in Emory’s Rollins School of Public Health. The team also included Gaylen Edwards and Kimberly Freeman at the University of Georgia.
The work was funded in part by the National Institutes of Health.
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What Did The Research Involve
The research was in human embryonic stem cells. The researchers tried two different techniques to try to get the stem cells to develop into BFCNs. First, they treated some of the cells with a sequence of chemicals known to promote the formation of nerve cells and to play a role in the developing forebrain. Second, they introduced DNA into other cells. This DNA carried instructions for making two proteins called Lhx8 and Gbx1, which control the development of BFCN cells. These proteins, called transcription factors, control the switching on of other genes.
The researchers then looked at whether cells treated in either way developed the characteristics of basal forebrain cholinergic neurons , for example, whether the genes they had switched on were typical of BFCNs. They also looked at whether the cells could make connections with other nerve cells if they were grown with slices of mouse brain in the laboratory.
Which Types Of Memory Are Affected By Alzheimers
Millions of adults live with Alzheimers disease. The disorder is most commonly recognized for causing memory loss. The protein tangles and subsequent inflammation damage the neurons in the regions of the brain that enable short-term and long-term memory, and the types of memory affected are further divided into subcategories.
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Dendritic Spine Density Analysis
To study the morphology of dendritic spines in hippocampal pyramidal neurons, brains were removed from the skull and impregnated with a Golgi-Cox solution. Brains were first immersed in a 5% Cr2K2O7, 5%Cl2Hg and 5% CrK2O4 solution for 6 days, then moved to a 30% sucrose solution for 35 days and finally sliced in 100m coronal sections at the CA1 level . Slices were sequentially washed with the following solutions: distilled water , H5NO , distilled water , Kodak Fix-film , distilled water , sequentially in 50, 70 and 95% alcohol , twice in 100% alcohol , in a solution of one-third xylene, one-third chloroform and one-third 100% alcohol , xylene . Slices were then coverslipped with Canada Balsam. The stained slices were analysed under a × 100 oil-immersion objective . During morphological analysis the specimen identity was unknown. A hippocampal pyramidal neuron was processed for morphological analysis if labelling was uniform, reaction precipitates were absent, if it did not overlap with neighbouring cells, if spines were clearly visible, dendritic arbours were relatively parallel to the section plane and arbours in distal dendritic branches were intact and visible. With these criteria, 30 CA1 pyramidal neurons were selected per group . The basal and apical dendritic arbours of each cell were examined separately using the softwares Sholl Analysis tool. Terminal spine density was calculated as number of spines along a 25m dendritic terminal segment.
Creating A Beneficial Environment For People With Dementia
People with dementia can benefit from an environment that is the following:
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Loss Of Microglial Phagocytic Abilities In Ad
Two-photon in vivo studies in the APP/PS1e9 and Tg2576 models demonstrated that removing microglia during the chronic disease stage causes significant growth of existing plaques . Combining these data with the fact that microglia are occasionally seen containing amyloid deposits led to conclude that while microglia may be competent phagocytes, they are unable to control amyloid levels late during AD pathology. Of note, the dark microglia are rare in the healthy mature brain, but increase in number up to 10-fold with pathological conditions that include chronic stress, aging and amyloid deposition . This microglial subset discovered with electron microscopy displays hyper-ramified processes that extensively ensheath and engulf synaptic elements , suggesting their role in the pathological remodeling of neuronal circuits in AD .
What Do We Already Know
Alzheimer’s disease affects brain cells known as neurons in specific regions of the brain that are involved in memory and thinking. Other cells in the brain are thought to have roles in the disease process as well, including specialised immune cells called microglia. However, the effects the disease has on other types of cells, particularly those in other regions of the brain, have not been thoroughly investigated.
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What Kind Of Research Was This
This laboratory study investigated whether researchers could manipulate stem cells to develop into a specific type of nerve cell that is lost early in the development of Alzheimers disease. These nerve cells are called basal forebrain cholinergic neurons . The loss of BFCNs is related to problems with spatial learning and memory. The researchers suggest that the ability to grow these brain cells in the laboratory could be a first step towards eventually using them to replace the lost cells in people with Alzheimers.
This type of research is important for developing techniques that may be useful in various ways. For example, cells generated in this way could be helpful in screening chemicals to identify those that might be helpful in preventing BFCN death in Alzheimers. Although, eventually, similar techniques might be used to generate cells for transplant into humans, much more research would be needed before this could be attempted.
Estimation Of Neuronal Densities
Densities of labeled neurons were estimated using a stereological method known as optical dissectors with the aid of Stereo Investigator software , using its Optical Fractionator tool. Neuronal densities, expressed as the number of labeled neurons per volume, were estimated in CA3, CA1, and subiculum, using Nissl-stained sections and NeuN-, PHFTau-AT8- and PHFTau-pS396-immunostained sections. Nissl-stained and NeuN-immunostained sections were used to identify the boundaries within the hippocampus.
After randomly selecting a starting point, six sections were chosen at equally spaced intervals. Optical dissectors were made with an oil immersion ×100 objective for both the NeuN-immunostained and Nissl-stained sections, on an average surface of 2,050 m2. The depth of the optical dissectors was 10 m, rendering a study volume of 20,500 m3 per optical dissector. An ×40 objective was used for the PHFTau-immunostained sections, on a surface of 14,450 m2. The depth of the optical dissectors in this case was also 10 m, rendering a study volume of 144,500 m3. Stereological parameters for each sample and neuronal marker were chosen. Since most neurons are located in the pyramidal cell layer, neuronal densities were estimated in this layer in the CA subfields and subiculum. In Nissl-stained sections, a neuron was only counted if the nucleolus was clearly identified in the optical plane along the vertical z-axis .
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Daergic Neuron Degeneration In The Vta At Pre
Figure 1: Tg2576 mice show selective loss of VTA DAergic neurons starting at 3 months of age.
Coronal brain section from a 6-month-old WT mouse showing intense TH immunoreactivity in the VTA and SNpc. Sections were Nissl-counterstained . The dashed line indicates the anatomical boundaries separating the VTA from the SNpc . On the right are higher magnification images showing TH+ and Nissl-counterstained neurons in the VTA and SNpc of WT and Tg2576 mice . The bar graphs show stereological quantification of TH+ and TH cell numbers in the VTA and SNpc in WT and Tg2576 mice at the indicated ages . DAergic neuronal loss in Tg2576 mice is selective for the VTA with the onset at 3 months of age . Data represent mean±s.e.m.
Finally, we investigated whether the selegiline treatment could restore the defects in CPP and food consumption observed in Tg2576 mice during the CPP test . As expected, although saline-treated Tg2576 animals were unable to show increased preference for the chamber associated with the rewarding food and consumed less chocolate during the conditioning phase, these deficits were absent from selegiline-treated mice . We conclude that the increased availability of DA in the hippocampus and NAc can ameliorate mnesic deficits and impairment in mesolimbic reward processing in 6-month-old Tg2576 mice.
What Neurological Problems Are Involved In Dementia
For neurons to function well, be replaced with healthy cells, and avoid premature cell death, key biological processes must occur. People with Alzheimers disease experience changes that impair critical functions:
- Communication between nerve cells. Neurons exchange information through a chemical-electric charge that crosses a microscopic gap called a synapse. A single healthy neuron may have as many as 7,000 synaptic connections to other nerve cells2.
- Regeneration and repair. Neurons have the ability to be repaired and to adjust or change their synaptic connections based on the chemical and electrical messages they receive. A healthy brain can even generate new nerve cells by the process of neurogenesis. This ability to repair or change connections and generate new cells is vital to memory and learning2.
- Nutrient delivery and metabolism. Nerve cells need a steady supply of chemicals and nutrients to perform their functions and survive. Oxygen and glucose are critical to cell survival, and good circulation delivers these key nutrients while carrying away the waste products of energy metabolism2.
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Estimations Of Amyloid Plaque Density And Volume
The number of A-ir plaques per volume was also estimated by the Optical Fractionator tool in DG, CA3, CA1 and subiculum . A minimum of six sections were selected for each patient, with equal intervals with an ×40 objective on a surface of 22,500 m2 and with a dissector depth of 10 m, rendering a study volume of 225,000 m3 per optical dissector.
To estimate the A-ir plaque volume, the edges of the plaque were delineated with the Nucleator tool with the aid of Stereo Investigator software . This tool provides the volume of each A-ir plaque analyzed, as well as the relative volume occupied by them in each examined hippocampal subfield to provide the percentage of tissue occupied by A-ir plaques.
Emotion And Behavior Treatments
The emotional and behavioral changes linked with Alzheimers disease can be challenging to manage. People may increasingly experience irritability, anxiety, depression, restlessness, sleep problems, and other difficulties.
Treating the underlying causes of these changes can be helpful. Some may be side effects of medications, discomfort from other medical conditions, or problems with hearing or vision.
Identifying what triggered these behaviors and avoiding or changing these things can help people deal with the changes. Triggers may include changing environments, new caregivers, or being asked to bathe or change clothes.
It is often possible to change the environment to resolve obstacles and boost the persons comfort, security, and peace of mind.
The Alzheimers Association offer a list of helpful coping tips for caregivers.
In some cases, a doctor may recommend medications for these symptoms, such as:
- antidepressants, for low mood
develops due to the death of brain cells. It is a neurodegenerative condition, which means that the brain cell death happens over time.
In a person with Alzheimers, the brain tissue has fewer and fewer nerve cells and connections, and tiny deposits, known as plaques and tangles, build up on the nerve tissue.
Plaques develop between the dying brain cells. They are made from a protein known as beta-amyloid. The tangles, meanwhile, occur within the nerve cells. They are made from another protein, called tau.
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Alzheimer’s And Dementia: Which Areas Of The Brain Are Affected
The human brain is made of billions of specialized cells designed to process and transmit information. When these cells lose their ability to function properly, vital communication between neurons is impaired or completely interrupted.
Dementia and Alzheimers disease disrupt neurons and cause damage to many areas of the brain, leading to a wide array of progressive symptoms. If you suspect dementia or Alzheimers in a loved one, it is important to find a neurologist to diagnose the cause of these cognitive and behavioral changes.
Before identifying the specific brain changes and the areas of the brain which are affected by Alzheimer’s, its important to define neurology terms to better understand this disease.
Loss Of Neuronal Connections And Cell Death
In Alzheimers disease, as neurons are injured and die throughout the brain, connections between networks of neurons may break down, and many brain regions begin to shrink. By the final stages of Alzheimers, this processcalled brain atrophyis widespread, causing significant loss of brain volume.
Learn more about Alzheimer’s disease from MedlinePlus.
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What Does This Project Involve
Dr Soreq will closely investigate the effect of Alzheimer’s disease on different types of cells in various areas of the brain. She will use a variety of techniques, including data analysis and genetic, computational and imaging technologies to find out the differences between these types of cells at the molecular level and in aspects such as size and shape. She will examine the differences in these cells between people with Alzheimer’s disease and those who are not affected by the condition.
Tau Accumulation And Selective Vulnerability Of The Lc Neurons
The accumulation of NFTs in AD follows a progressive, predictable pattern throughout the disease process with regards to their severity and location in the cortex, known as Braak stages I-VI. At stage I, NFTs are observed in the transentorhinal cortex at stage II, NFTs are found in the entorhinal cortex hippocampal coverage occurs at stage III which then additionally affects the basal, frontal and insular cortex by stages IV and V by stage VI, the primary sensory and motor areas become affected . Cognitive symptoms are not experienced until stage III or IV where the NFTs affect the hippocampus and therefore tau pathology occurs prior to symptom onset. Immunostaining human tissue with the antibody AT8 to visualize hyperphosphorylated tau , has demonstrated that abnormal tau accumulates in the LC prior to NFTs being visualized in the transentorhinal cortex , at an early age, i.e., before 30 years, decades before disease onset . The LC seems to be particularly vulnerable to early tau pathology and stages a, b, and c have been added to the Braak staging system to describe the accumulation of p-tau in the LC and other subcortical nuclei preceding stages I-IV. This occurs both before cognitive impairment and the onset of LC cell loss which is not significant until Braak stage III .
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