neurological disorder Archives - Amazing Health Advances

When Your Loved One has Aphasia

The AHA! Team — Mon, 28 Jul 2025 05:28:22 +0000

Meredith Nye, CCC-SLP, MS, via Duke Health – Speech pathologists can help relatives and friends work with a loved one who has aphasia and find ways to communicate effectively. Aphasia is a language disorder that can affect comprehension and communication. Although it is most often caused by a stroke, aphasia can also result from traumatic brain injury, brain tumors, or progressive neurological disorders such as primary progressive aphasia (PPA). These conditions damage the language centers of the brain, leading to difficulties with speaking, understanding, reading, and/or writing. Learning to communicate with someone who has aphasia can positively impact that person’s social interactions, relationships, medical decision-making, and overall wellbeing. “We work with patients and their care partners to provide customized treatment plans focusing on life participation and maximizing communication success,” says Meredith Nye, CCC-SLP, MS, a Duke speech-language pathologist. “Aphasia doesn’t impact a person’s hearing or thinking skills like memory. Rather,” she says, “people with aphasia may use the wrong word, like ‘mother’ instead of ‘daughter’ or ‘yes’ instead of ‘no.’ Or they may make up words, unintentionally repeat themselves, or only be able to say a few words or sounds when they are trying to communicate. Or they may have a hard time understanding what you’re saying.” How to Communicate with Someone with Aphasia Speech pathologists can help relatives and friends work with a loved one who has aphasia and find ways to communicate effectively. Nye recommends keeping these tips in mind: Focus Their Attention If possible, move your conversation to a quiet, well-lit room where there are no distractions. Turn off background disturbances like the radio or television. It’s best to limit conversation to one or two people at the most. Use All Forms of Nonverbal Communication Rather than rely on words, use a wave to say “goodbye” or “hello.” Thumbs up can be used to say “good job” or “yes.” Your facial expressions can show anger, sadness, or elation. Exchange written or drawn messages. Have Patience Sometimes it takes longer for a person with aphasia to communicate. Count to 10 slowly before providing help or choices. Many times it takes that much time or longer for them to get their message out. Confirm Your Understanding After an exchange with your loved one, make sure you understand by verbally repeating or by writing a synopsis of the message’s key points. If they wanted coffee, write “coffee” and draw a picture. Use intonation in your voice when you ask, “You want coffee?” and point to the picture. Have them answer yes or no. Use Technology Computers, smart devices, and other forms of technology can help people with aphasia return to hobbies, read, and converse with others. Icons and emojis can enhance email and social media conversations. Encourage your loved one to listen to audiobooks in addition to reading the print versions. Speech pathologists can also recommend programs that enable your loved one to use word-prediction or speech-to-text capabilities. Get Help Speech pathologists can help people make progress even years after they are originally diagnosed with aphasia, says Nye. “We can help them focus on their strengths and find ways to better engage with family and their community. We can offer tools to help them socialize and have a better quality of life through communication.” Find Aphasia Support Groups There are many groups and resources in the community to support people with aphasia and their families. Nye says a speech-language pathologist is your best resource for identifying groups in your area. To read the original article click here.

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Saffron Put to the Test for Alzheimer’s

AHA Publisher — Thu, 17 Jun 2021 07:00:56 +0000

Michael Greger M.D. FACLM via Nutrition Facts – The spice saffron is pitted head-to-head against the leading drug for severe Alzheimer’s disease. What’s the latest on treating memory disorders with the spice saffron? As I discuss in my video Saffron Versus Memantine (Namenda) for Alzheimer’s, “saffron has been widely used in the Persian traditional medicine for memory problems,” but it wasn’t put to the test until a study showed that Alzheimer’s dementia symptoms continued to worsen on placebo but got better on saffron over a 16-week period, as you can see at 0:21 in my video. The researchers concluded that saffron is “safe and effective in mild-to-moderate AD [Alzheimer’s disease] patients,” at least in the short term. What about head-to-head against the leading drug used for such patients? Saffron appeared to work just as well—but with significantly less vomiting, a common side effect of the drug in this study. So, that’s where we were as of 2010. What’s the update? In 2013, we got the first glimpse of a potential mechanism. Alzheimer’s disease involves “brain nerve cell destruction.” Our brain cells can be killed by the buildup of either tangles or amyloid plaques, where aggregates of a protein called amyloid beta “act as a poison.” But, as you can see at 1:13 in my video, adding crocin, the red pigment found in saffron, significantly reduces this amyloid clumping in a petri dish, which is an effect that can be plainly seen under an electron microscope. So, the component of saffron that makes it so colorful appears to have “the ability to prevent amyloid formation.” What about the tangles? Crocin also seems to be able to block the tangles in vitro, as demonstrated once again with electron microscopy. Perhaps this is why saffron helps in Alzheimer’s disease, but this was just for mild-to-moderate Alzheimer’s. Does that mean you have to catch it early? What about moderate-to-severe Alzheimer’s? We didn’t know, until a study compared saffron head-to-head against the leading drug for severe Alzheimer’s. Once again, saffron seemed to work just as well, as you can see at 2:01 in my video. In fact, one might consider saffron worked even better because there haven’t been any serious adverse effects attributed to saffron, whereas the drug is associated with increased risk of sleepiness, weight gain, confusion, hypertension, nervous system disorders, and falling. The saffron study wasn’t funded by supplement or spice companies—just noncommercial public grants. But, all the studies were done in Iran, which controls about 90 percent of the saffron crop. So, promoting saffron consumption may be of national interest, just like the New Zealand government funds research on kiwifruit—though who else is going to fund studies on a simple spice? To read the original article click here. For more articles from Dr. Greger click here.

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Understanding Gut Inflammation May Hold Clues to Mitigating Parkinson’s Onset

AHA Publisher — Mon, 14 Jun 2021 07:00:31 +0000

Van Andel Research Institute via EurekAlert – GRAND RAPIDS, Mich. (JUNE 8, 2021) — Chronic inflammation in the gut may propel processes in the body that give rise to Parkinson’s disease, according to a study by scientists at Van Andel Institute and Roche. The study, published in Free Neuropathology, is the latest in a growing list that links the gut and the immune system to Parkinson’s. The researchers’ findings in an experimental mouse model of gut inflammation track with several large-scale epidemiological studies that show an association between Parkinson’s and inflammatory bowel diseases, such as ulcerative colitis and Crohn’s disease. Epidemiological evidence from other groups indicates the risk of developing Parkinson’s fades in certain people whose inflammatory bowel disease is treated with anti-TNF, a standard-of-care anti-inflammatory therapy, which suggests that reducing gut inflammation may have promise for mitigating Parkinson’s onset. “There is increasing evidence that changes in the gut can affect a variety of neurological and psychiatric brain disorders,” said Patrik Brundin, M.D., Ph.D., VAI deputy chief scientific officer and co-corresponding author of the study. “Parkinson’s is a complex disease with a wide range of factors that work in concert to spark its onset and progression. We need to understand the gut’s likely influence on Parkinson’s development better. This study provides novel insights, and this new knowledge can facilitate the development of improved treatment approaches.” In their disease models, the team found that chronic gut inflammation triggers a protein called alpha-synuclein to clump together in walls of the colon, as well as in local immune cells called macrophages. A similar process may play out in the colons of some people — such as those with inflammatory bowel diseases — thereby increasing their risk to develop Parkinson’s as shown in studies by other groups. Similarly, in the brains of people with Parkinson’s, “sticky” alpha-synuclein aggregates also develop. For reasons that still are unclear, these aggregates can clog the molecular machinery that keep neurons alive. The resulting loss of some of these critical cells — and the chemical messenger they produce called dopamine — causes Parkinson’s hallmark movement-related symptoms, such as freezing and loss of voluntary movement. The additional wide-spread development of alpha-synuclein aggregates throughout the brain also may be associated with the disease’s non-motor symptoms and may fuel its progression, which cannot be slowed or stopped with existing treatments. The study also revealed that chronic inflammation in the gut early in life can exacerbate alpha-synuclein clumping throughout the brain in older mice. While it isn’t clear exactly how this happens, the team has two theories: first, they suggest inflammatory chemicals may travel from the gut to the brain via the bloodstream, triggering a runaway inflammatory immune response that leads to protein aggregation. Another idea is that alpha-synuclein aggregates may travel to the brain via the vagus nerve, one of the longest nerves in the body and a “superhighway” between the gut and the brain. Once there, the proteins may then execute their toxic activity in the brain. “We now know that systems throughout the body contribute to Parkinson’s,” said Emmanuel Quansah, Ph.D., a postdoctoral fellow in Brundin’s lab and a key contributor and co-author of the study. “It was striking to see protein aggregation pathology in the brain that mirrored pathology in the colon brought on by inflammation. A particularly intriguing observation was the loss dopamine-producing nerve cells — which play a major role in Parkinson’s onset — in our models that had gut inflammation a year-and-a-half earlier.” Notably, the team also found that modulating immune activation in the colitis mouse model by genetic or therapeutic means tuned the level of alpha-synuclein clumps in the colon up or down. “Our results in mice, together with the genetic and epidemiological data by others in humans, make a strong case for further exploring systemic immune pathways for future therapies and biomarkers for Parkinson’s,” said Markus Britschgi, Ph.D., Senior Principal Scientist and Section Head in the Neuroscience and Rare Diseases Research Department at the Roche Innovation Center Basel and co-corresponding author of the study. Authors include first author Stefan Grathwohl, Ph.D. (previously a Roche postdoctoral fellow), Nazia Maroof, Ph.D. (previously a Roche postdoctoral fellow), Liz Spycher, Krisztina Oroszlan-Szovik, M.S., Helga Remy, Markus Haenggi M.S., and Marc Stawiski of Roche Pharma Research and Early Development, Neuroscience and Rare Diseases Discovery and Translational Area, Roche Innovation Center Basel; Jennifer A. Steiner, Ph.D., Zachary Madaj, M.S., and Martha L. Escobar Galvis, Ph.D., of VAI; Fethallah Benmansour, Ph.D., of Roche Pharma Research and Early Development, pREDi, Roche Innovation Center Basel; Gonzalo Duran-Pacheco, Ph.D., Juliane Siebourg-Polster, Ph.D., Matthias Selhausen, Pierre Maliver, EVCP, Arel Su, DVM, and Annika Herrmann, DECVP, of Roche Pharma Research and Early Development, Pharmaceutical Sciences, Roche Innovation Center Basel; Andreas Wolfert and Thomas Emrich, Ph.D., of Roche Pharma Research and Early Development, Pharmaceutical Sciences, Roche Innovation Center Munich; and Christoph Mueller, Ph.D., of Institute of Pathology, University of Bern. To read the original article click here.

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