Serotonergic Degeneration In Pd And Als
Staging of brain pathology in PD demonstrated an early involvement of Lewy body depositions within the RN. In more detail, Halliday et al. firstly described a 56% loss of serotonergic neurons in the median RN of PD compared to control brain. Afterwards, Braak et al. determined six stages in the evolution of PD-related pathology, with lesions being present in the median RN in the caudal brainstem already from stage two onwards. Furthermore, 5-HT depletion was observed in various target areas of the RN, such as in the basal ganglia, hypothalamus, hippocampus, and prefrontal cortex . This was later confirmed by in vivo imaging studies, revealing new insights. For instance, Politis et al. applied 11C-DASB-PET to early-stage PD patients, and demonstrated reduced SERT binding in the caudate nucleus, thalamus, and anterior cingulate cortex, whereas PD subjects with established disease showed additional 11C-DASB binding reductions in the putamen, insula, posterior cingulate cortex, and, prefrontal cortex. Further binding reductions were noticed in the ventral striatum, RN, and amygdala of advanced PD patients. Interestingly, the loss of SERT binding in the RN occurred in later stages, pointing to an earlier loss of serotonergic projections instead of the neurons themselves.
Als And Parkinsons Symptoms
- This topic has 3 replies, 4 voices, and was last updated 3 years, 1 month ago by
Is anyone experience the Parkinson symptoms?
- April 13, 2019 at 1:45 am#11435Participant
Parkinson is a terrible disease, and the price on carers is high.
There was recently an article in Science about lack of results in terms of effective treatments in humans in Alzheimer research.
The main message was that when people are old, they have many conditions. So any research that try to target something specific will fail to succeed, merely because brain cells die for one reason or another and there are many.
- April 14, 2019 at 5:46 pm#11447Dagmar MunnKeymaster
Alzheimers, Parkinsons, ALS and more you are correct Jean-Pierre, it is a challenge for researchers when our bodies are a moving target.
- May 30, 2019 at 7:55 pm#12196
Genetics Of Ftd And Als
A wide spectrum of genes encompassing diverse pathogenic variants has been found to be associated with FTD, ALS and FTD-ALS. Although there is a causal relationship between gene mutations and the pathogenesis of the diseases, there is, on the other hand, abundant evidence of cases with specific pathology lacking mutations in the genes encoding these proteins: this fact could imply that mutations contribute partially to pathogenesis exerting their influence on pathogenic pathways that lead to the disease rather than being the direct cause of the disease. Genetics of the two disorders and overlaps are discussed in the following sections.
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Do Ms And Als Have The Same Risk Factors
Age is risk factor for both ALS and MS, but ALS usually is diagnosed in older individuals , with an average age of onset of 55. While MS is diagnosed in a younger population .
ALS is more common in men by about 20%, while MS is about 2 to 3 times more likely to develop in women.Heredity plays a significant role in some individuals that develop ALS . MS is not considered to be a hereditary disease, but new data may modify this conclusion.
In addition, being a member of the military raises the risk of developing ALS. However, military service is not considered a risk factor for MS.
If you have an identical twin with MS, there is a 30% chance for you to develop MS.
Treatment Of Als Vs Parkinsons Disease
There is currently no cure for ALS and much of the treatment is aimed at managing the symptoms and trying to slow down the progression of the disease. Ultimately the disease will be fatal and once bodily functions such as swallowing and breathing are affected, the prognosis is very poor.
Typically, around half of those diagnosed with ALS will die within the first three years following their diagnosis. Only 10% of those diagnosed will live beyond 10 years.
Treatment of Parkinsons disease has received a lot more attention with its higher profile in the media. As with ALS, there is currently no cure but there are a wide range of different medications and treatments that are available.
This includes brain stimulation therapy which sends an electrical stimulus to the brain from a device embedded by the collarbone to help alleviate symptoms such as tremors.
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So What’s The Difference Between Als And Parkinson’s Disease
Clockwise from top left: Robin Williams had been diagnosed with Parkinsons before his death Stephen Hawking has been living with ALS for 50 years Lou Gehrig brought ALS, now also know as Lou Gehrigs disease, to the publics attention and Michael J. Fox received his Parkinsons diagnosis in 1992.
News that Robin Williams had been grappling with a diagnosis of Parkinsons disease before ending his life has sparked increased interest in the disorder this week. And thats coincided with a fast-rising awareness of a similar disease amyotrophic lateral sclerosis, or ALS due to the Ice Bucket Challenge, a fundraising campaign thats swept social media recently, prompting everyone from Ethel Kennedy to Justin Timberlake to dump freezing water over their heads in the name of research. So how closely linked to Parkinsons is ALS? Both are progressive neurodegenerative diseases, and neither has a cure. But beyond that, the differences are vast.
Both occur because some cells in the brain degenerate, and both are diseases of the motor system, meaning they affect how someone moves, Dr. U. Shivraj Sohur, a movement disorder specialist with the MassGeneral Institute for Neurodegenerative Disease, told Yahoo Health. From there, the separation happens quickly, both from a neurology point of view and from a patients experience.
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Yales Unique Approach To Neurodegenerative Disease Research
Grappling with the complexities of neurodegenerative disease requires patience, creativity, and a willingness to consider new perspectives. These researchers work is a testament to Yales fostering of interdisciplinary partnerships in which cell biologists, geneticists, basic neuroscientists, and clinicians cooperate to answer fundamental questions about disease and consider therapeutic innovations. A unique feature of Yale research on neurodegeneration is that it is anchored within a very strong cell biology community, said de Camilli.
These efforts have led to initiatives like the Program in Cellular Neuroscience, Neurodegeneration and Repair, with broad research support provided from within the Kavli Institute for Neuroscience. Its been exciting to see Yales growing commitment to neurodegenerative disease research on many levels, especially in basic science that complements clinical research, van Dyck said.
Yale is a great place for multidisciplinary investigations, said Strittmatter. We have a launch pad to bring many labs together. I think were well positioned to make a difference by approaching neurodegeneration and repair from multiple perspectives, taking genetic and pathologic data, designing therapeutics, and ultimately making a clinical impact.
Originally published Spring 2020 updated May 10, 2022
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How Do Als And Ms Affect You Mentally
For people with ALS, symptoms remain largely physical. In fact, in many people with ALS, mental function remains intact even when most of their physical capabilities have been affected.
However, according to the ALS Foundation, its been estimated that up to 50 percent of people with ALS may experience some mild to moderate cognitive or behavioral changes due to the disease.
As it progresses, some people have gone on to develop dementia.
In MS, mental capabilities are usually more affected than in ALS.
People with MS can experience severe mental changes, including:
- mood shifts
The Challenge Of Neurodegenerative Diseases
Today, 5 million Americans suffer from Alzheimer’s disease 1 million from Parkinson’s 400,000 from multiple sclerosis 30,000 from amyotrophic lateral sclerosis , and 30,000 from Huntington’s disease. Because neurodegenerative diseases strike primarily in mid- to late-life, the incidence is expected to soar as the population ages. If left unchecked 30 years from now, more than 12 million Americans will suffer from neurodegenerative diseases. Finding treatments and cures for neurodegenerative diseases is a goal of increasing urgency.
In recent years, scientists of the Harvard NeuroDiscovery Center and many others have made great strides in understanding the underlying causes of neurodegenerative diseases. As we uncover more details of these diseases, we are confident that in time we will be able to treat and prevent them. But as for most major endeavors, the greater the resources we bring to bear, the faster the progress toward our goal. If as a community we want to avoid the looming and dramatic impact of these diseases on our increasingly elderly population, we must all redouble our efforts, now.
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Parkinsons Disease May Share Sod1 Protein Anomaly With Als Study Finds
Parkinsons disease and amyotrophic lateral sclerosis may have more in common than previously thought. According to a recent study, a known ALS gene called SOD1 also may be involved in the development of Parkinsons.
This finding opens the possibility of treating Parkinsons patients with therapies targeting SOD1 toxicity, which already have been investigated in clinical trials for ALS.
The study, Amyotrophic lateral sclerosis-like superoxide dismutase 1 proteinopathy is associated with neuronal loss in Parkinsons disease brain, was published in the journal Acta Neuropathologica.
ALS is a neurodegenerative disease marked by loss of motor neurons, which control the muscles in the body. Previous studies have shown that about 20% of familial ALS cases carry mutations in the gene encoding SOD1. These mutations are responsible for the faulty folding of the protein, which then aggregates in the brain, leading to impairment of motor neurons and ALS symptoms.
Now, researchers have found that abnormal SOD1 also may be involved in the development of Parkinsons disease, leading to the formation of protein aggregates that closely resembles that of neurotoxic SOD1 deposits in SOD1-associated familial amyotrophic lateral sclerosis , researchers wrote.
The team also found that these aggregates of faulty SOD1 promote neuronal impairment and copper deficiency in the brain, similar to that seen in mutant SOD1 in fALS.
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Understanding The Differences Between Parkinsons And Lou Gehrigs Disease
By Angie Kunnath 7 pm on June 5, 2015
As Parkinsons disease and Amyotrophic Lateral Sclerosis are both progressive neurodegenerative diseases, many people confuse the terms. Below, senior care experts at Home Care Assistance of Mississauga provide information on the basic differences between Parkinsons and ALS to help you better understand the two diseases.
Difference Between Parkinsons Disease And Als Signs And Symptoms
Parkinsons disease typically begins with tremors, followed by muscle stiffness, difficulty standing or walking, changes in speech, slow movements, impaired posture and balance, loss of automatic movements, and writing changes.
Signs and symptoms of ALS include slurred speech, hoarseness, difficulty swallowing, emotional liability , loss of tongue muscle contour, excess saliva, difficulty breathing, limp muscles or flaccid weakness, muscle wasting, and twitching.
In the early stages of the disease, ALS patients may notice that performing regular everyday tasks has become more challenging. For example, they may experience difficulty climbing steps or getting up from a chair. Symptoms may first begin on one side of the body, but as the condition progresses, they spread to both sides.
As you can see, ALS and Parkinsons disease share symptoms associated with the negative impact of both conditions on movement and muscle function.
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Alterations In Other Monoamine Neurotransmitter Systems
NA levels have been previously reported to be significantly increased in the cervical, thoracic and lumbar spinal cord of ALS patients compared to controls , with highest concentrations measured in ventral and intermediate gray matter. In CSF, a similar increase has been noted . Independently of 5-HT, NA increases the excitability of motor neurons to glutamate . Bertel et al. further discussed that in all probability, it is unlikely that the noradrenergic changes were due to the effect of tissue shrinkagesince concentrations were expressed in ng/g wet weighed tissuebut rather a consequence of denser noradrenergic innervation, such as from sprouting of noradrenergic fibers into affected areas. In PD, the noradrenergic dysfunction has been investigated in more detail. In summary, -synuclein depositions in the locus coeruleus , the brain’s main source of NA, have been evidenced to precede that of the SN . Consequently, neuronal loss in this noradrenergic nucleus and the accompanying noradrenergic deficiency both on the central and peripheral level have been related to various motor and non-motor symptoms, including the progression to dementia .
What Makes Them Different
MS and Parkinsonâs have different causes. They usually start to affect you at different ages, too.
MS often affects people between ages 20 and 50, but children get it, too. Parkinsonâs usually starts at age 60 or older, but some younger adults get it.
MS is an autoimmune disease. That means your bodyâs immune system goes haywire for some reason. It attacks and destroys myelin. As myelin breaks down, your nerves and nerve fibers get frayed.
In Parkinsonâs, certain brain cells start to die off. Your brain makes less and less of a chemical called dopamine that helps control your movement. As your levels dip, you lose more of this control.
Some genes may put you at risk for Parkinsonâs, especially as you age. Thereâs a small chance that people who are exposed to toxic chemicals like pesticides or weed killers can get it, too.
These symptoms are more common if you have MS. They not usually found in Parkinsonâs:
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The Role Of Lysosomes In Alzheimers Disease
Shawn Ferguson, PhD, associate professor of cell biology and of neuroscience, has taken a different approach to understanding the consequences of these mutations. What if the problem isnt just that theres a buildup of misfolded proteins, he asks, but rather that the cell is unable to dispose of them once theyve aggregated?
Fergusons lab studies lysosomes, the organelles tasked with degrading macromolecules to clear cellular waste and recycle nutrients. Lysosomes are particularly crucial in neurons, given the longevity expected of the cells. Moreover, the extreme size of neurons also presents challenges as these cells must also ensure that lysosomes are properly distributed over long distances. Genes encoding lysosomal pathway proteins have been flagged as risk factors for inherited neurodegenerative diseases, but the pathological impactconsistent with other conditions associated with agingis incremental. Were looking at the long-term consequences of relatively subtle defects, Ferguson said.
Ferguson hopes that the research will reveal ways to restore lysosome transport and function. Understanding how lysosomes are transported in axons to meet the extreme demands of neurons can help us develop strategies to enhance this process for the treatment and prevention of Alzheimers disease, said Ferguson.
Prognosis Of Als Vs Parkinsons
ALS is considered as a fatal disease. The damage and death of neurons begins to spread throughout the body. In the later stages, nerve damage will affect areas like breathing and swallowing.
Parkinsons disease in itself is not considered fatal but people do die from complications relating to the condition.
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Dementia With Lewy Bodies
DLB is second only to Alzheimers as the most common cause of dementia in the elderly. It causes progressive intellectual and functional deterioration. In addition to the signs and symptoms of Parkinsons disease, people with DLB tend to have frequent changes in thinking ability, level of attention or alertness and visual hallucinations. They usually do not have a tremor or have only a slight tremor. The parkinsonian symptoms may or may not respond to levodopa.
Serotonergic Modulation Of Basal Ganglia And Mesencephalic Dopaminergic Activity In Pd
The basal ganglia are composed of the striatum , subthalamic nucleus , internal and external globus pallidus and SN, and are part of the BG-cortico-thalamic circuits. This highly organized network is important for motor control, emotion, and cognition. It has been firmly established that BG nuclei receive vast serotonergic input mainly coming from the rostral RN clusters , with effects on mesencephalic dopaminergic activity depending on the specific nucleus and its receptor distribution . In PD, lesioning of the RN in addition to DA depletion in the striatum and SNparticularly of the pars compacta are hallmarks of the disease, leading to overactivation of the output regions of the BG, i.e., GPi and SN pars reticulata , which contain large GABAergic neurons. This cascade results in a net decreased activity of the supplementary motor areas, premotor, and primary motor cortices, triggering parkinsonian symptoms . Overall, the loss of 5-HT neurons is not as profound as the loss of DA neurons, and may not be sufficient to cause motor or non-motor symptoms per se, however, both systems closely interact, and combined depletion certainly seems to aggravate the situation, as was shown in a parkinsonian rat model . Moreover, 5-HT and 5-HIAA levels, as well as SERT expression, are reduced in various BG nuclei , and the serotonergic system is strongly involved in the mechanism of action of antiparkinsonian therapeutics, such as levodopa , and high frequency stimulation of the STN .
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Cognitive/behavioural Manifestations Before Phenoconversion To Amyotrophic Lateral Sclerosis
Frontotemporal spectrum dysfunction in amyotrophic lateral sclerosis
Prodromal mild cognitive impairment
Our conceptual framework for characterizing MCI differs somewhat from that used by the FTD community, which relies heavily on the clinical judgement of a behavioural neurologist, combined with subjective informant report and results of neuropsychological testing. By contrast, in the study of pre-symptomatic ALS, we rely on formal objective neuropsychological assessment, conducted or supervised by a qualified neuropsychologist, as the principal means for assessing cognition. This approach is informed by the practical consideration that ALS neurologists may feel less comfortable than cognitive/behavioural neurologists in relying on clinical judgements of MCI. In addition, while subjective cognitive complaints may manifest in the prodromal stage, such symptoms may also be non-specific and of uncertain significance. Moreover, subjective cognitive complaints may be absent despite clinically significant cognitive decline due to limited awareness. We have, therefore, elected to classify those with only subjective cognitive symptoms as uncertain, and those with deficits on neuropsychological testing or where clinically meaningful decline on neuropsychological testing is detected among those with high premorbid functioning, as MCI.
Prodromal mild behavioural impairment
Differentiating mild from uncertain