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文章數：85 |
 加分100%浜中特選昆布鍋物家庭過節聚會適合嗎？》公益路必吃Top10｜美食路線一次規劃好 |
| 興趣嗜好｜偶像追星 2026/04/18 22:27:36 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
身為一個熱愛美食、喜歡在城市裡挖掘驚喜的人，臺中公益路一直是我最常出沒的地方之一。這條路可說是「臺中人的美食戰場」，從精緻西餐到創意火鍋，從日式丼飯到義式早午餐，每走幾步，就會有完全不同的特色料理餐廳。 這次我特別花了一整個月，實際造訪了公益路上十間口碑不錯的餐廳。有的是網友熱推的打卡名店，也有隱藏在巷弄裡的小驚喜。我以環境氛圍、口味表現、價格CP值與再訪意願為基準，整理出這篇實測評比。希望能幫正在猶豫去哪裡吃飯的你，找到那一間「吃完會想再來」的餐廳。 評比標準與整理方向
這次我走訪的10家餐廳橫跨不同料理類型，從高質感牛排館到巷弄系早午餐，每一間都有自己獨特的風格。為了讓整體比較更客觀，我依照以下四大面向進行評比，並搭配實際用餐體驗來打分。
整體而言，我希望這份評比不只是「哪家好吃」，而是幫你在不同情境下（約會、家庭聚餐、朋友小聚、商業午餐）都能快速找到合適的選擇。畢竟，美食不只是味覺的滿足，更是一段段與朋友共享的生活記憶。 10間臺中公益路餐廳評比懶人包公益路向來是臺中人聚餐的首選地段，從火鍋、燒肉到中式料理與早午餐，每走幾步就有驚喜。以下是我實際造訪過的10間代表性餐廳清單，橫跨平價、創意、高級各路風格。
一頭牛日式燒肉｜炭香濃郁的和牛饗宴，約會聚餐首選
走在公益路上，很難不被 一頭牛日式燒肉 的木質外觀吸引。低調卻不失質感的門面，搭配昏黃燈光與暖色調的內裝，讓人一進門就感受到濃濃的日式職人氛圍。店內空間不大，但桌距規劃得宜，每桌皆設有獨立排煙設備，烤肉時完全不怕滿身油煙味。 餐點特色
一頭牛的靈魂，絕對是他們招牌的「三國和牛拼盤」。 用餐體驗整體節奏掌握得非常好。店員會在你剛想烤下一片肉時貼心遞上夾子、幫忙換烤網，讓人完全不用分心。整場用餐過程就像一場表演，從視覺、嗅覺到味覺都被滿足。 綜合評分
地址：408臺中市南屯區公益路二段162號電話：04-23206800 小結語一頭牛日式燒肉不僅是「吃肉的地方」，更像是一場五感盛宴。從進門那一刻到最後一道甜點，都能感受到他們對細節的用心。 TANG Zhan 湯棧｜文青系火鍋代表，麻香湯底與視覺美感並重
在公益路這條美食戰線上，TANG Zhan 湯棧 是讓人一眼就會想走進去的那一種。 餐點特色
湯棧最有名的當然是它的「麻香鍋」。 用餐體驗整體氛圍比一般火鍋店更有質感。 綜合評分
地址：408臺中市南屯區公益路二段248號電話：04-22580617 官網：https://www.facebook.com/TangZhan.tw/ 小結語TANG Zhan 湯棧 把傳統火鍋做出新的樣貌保留臺式鍋物的溫度，又結合現代風格與細節服務，讓吃鍋這件事變得更有品味。 如果你想找一間兼具「好吃、好拍、好放鬆」的火鍋店，湯棧會是公益路上最有風格的選擇之一。 NINI 尼尼臺中店｜明亮寬敞的義式早午餐天堂
如果說前兩間是肉食愛好者的天堂，那 NINI 尼尼臺中店 絕對是想放鬆、聊聊天的好地方。餐廳外觀以白色系與大片玻璃窗為主，陽光灑進室內，讓人一踏入就有種度假般的輕盈感。假日早午餐時段特別熱鬧，建議提早訂位。 餐點特色
NINI 的菜單融合義式與臺灣人口味，選擇多樣且份量十足。主打的 松露燉飯 濃郁卻不膩口，米芯保留微Q口感；而 香蒜海鮮義大利麵 則以新鮮白蝦、花枝與淡菜搭配微辣蒜香，口感層次豐富。 用餐體驗店內氣氛輕鬆不拘謹，無論是一個人帶電腦工作、或朋友聚餐，都能找到舒服角落。餐點上桌速度穩定，服務人員態度親切、補水與收盤都非常主動。整體節奏讓人覺得「時間變慢了」，很適合想遠離忙碌日常的人。 綜合評分
地址：40861臺中市南屯區公益路二段18號電話：04-23288498 小結語NINI 尼尼臺中店是一間能讓人放下手機、慢慢吃飯的餐廳。餐點不追求浮誇，而是以「剛剛好」的份量與風味，陪伴每個平凡午後。如果你在找一間能邊吃邊聊天、拍照也漂亮的早午餐店，NINI 會是你在公益路上最不費力的幸福選擇。 加分100%浜中特選昆布鍋物｜平價卻用心的湯頭系火鍋，家庭聚餐好選擇
在公益路這條高質感餐廳林立的戰場上，加分100%浜中特選昆布鍋物 走的是截然不同的路線。它沒有浮誇的裝潢、也沒有高價位的套餐，但靠著實在的湯頭與親切的服務，默默吸引許多回頭客。每到用餐時間，總能看到家庭或情侶三兩成群地圍著鍋邊聊天。 餐點特色
主打 北海道浜中昆布湯底，湯頭清澈卻不單薄，越煮越能喝出海藻與柴魚的自然香氣。 用餐體驗整體氛圍偏家庭取向，桌距寬敞、座位舒適，帶小孩來也不覺擁擠。店員態度親切，補湯、收盤都很勤快，給人一種「被照顧著」的安心感。 綜合評分
地址：403臺中市西區公益路288號電話：0910855180 小結語加分100%浜中特選昆布鍋物是一間「不浮誇、但會讓人想再訪」的火鍋店。它不追求豪華擺盤，而是用最簡單的湯頭與新鮮食材，傳遞出家常卻不平凡的溫度。 印月餐廳｜中式料理的藝術演繹，宴客與家庭聚會首選
說到臺中公益路的中式料理代表，印月餐廳 絕對是榜上有名。這間開業多年的餐廳以「中菜西吃」的概念聞名，把傳統中式料理以現代手法重新詮釋。從建築外觀到餐具擺設，每個細節都散發著低調的典雅氣息。 餐點特色
印月最令人印象深刻的是他們將傳統中菜融入創意手法。 用餐體驗服務方面完全對得起餐廳的高級定位。從入座、點餐到上菜節奏，都拿捏得恰如其分。每道菜都會有服務人員細心介紹食材與吃法，讓人感受到「被款待」的尊榮感。 綜合評分
地址：408臺中市南屯區公益路二段818號電話：0422511155 小結語印月餐廳是一間「不只吃飯，更像品味生活」的地方。 KoDō 和牛燒肉｜極致職人精神，專為儀式感與頂級味覺而生
若要形容 KoDō 和牛燒肉 的用餐體驗，一句話足以總結——「像在欣賞一場關於肉的表演」。 餐點特色
這裡主打 日本A5和牛冷藏肉，以「精切厚燒」的方式呈現。 用餐體驗KoDō 的最大特色是「儀式感」。 綜合評分
地址：403臺中市西區公益路260號電話：0423220312 官網：https://www.facebook.com/kodo2018/ 小結語KoDō 和牛燒肉不是日常餐廳，而是一場體驗。 永心鳳茶｜在茶香裡用餐的優雅時光，臺味早午餐的新詮釋
走進 永心鳳茶公益店，彷彿進入一間有氣質的茶館。 餐點特色
永心鳳茶的餐點結合中式靈魂與西式擺盤，無論是「炸雞腿飯」還是「紅玉紅茶拿鐵」，都能讓人感受到熟悉卻不平凡的味道。 用餐體驗店內服務人員態度溫和，對茶品介紹詳盡。上餐節奏剛好，不急不徐。 綜合評分
地址：40360臺中市西區公益路68號三樓(勤美誠品)電話：0423221118 小結語永心鳳茶讓人重新定義「臺味」。 三希樓｜老饕級江浙功夫菜，穩重又帶人情味的中式饗宴
位於公益路上的 三希樓 是許多臺中老饕的口袋名單。 餐點特色
三希樓的菜色以 江浙與港式料理 為主，兼顧傳統與現代風味。 用餐體驗三希樓的服務給人一種老派但貼心的感覺。 綜合評分
地址：408臺中市南屯區公益路二段95號電話：0423202322 官網：https://www.sanxilou.com.tw/ 小結語三希樓是一間「吃得出功夫」的餐廳。 一笈壽司｜低調奢華的無菜單日料，職人手藝詮釋旬味極致
在熱鬧的公益路上，一笈壽司 低調得幾乎不顯眼。 餐點特色
一笈壽司採 Omakase（無菜單料理） 形式，每一餐都由主廚根據當日食材設計。 用餐體驗整場用餐約90分鐘，節奏緩慢但沉穩。 綜合評分
地址：408臺中市南屯區公益路二段25號電話：0423206368 官網：https://www.facebook.com/YIJI.sushi/ 小結語一笈壽司是一間真正讓人「放慢呼吸」的餐廳。 茶六燒肉堂｜人氣爆棚的和牛燒肉聖地，肉香與幸福感同時滿分
若要票選公益路上「最難訂位」的餐廳，茶六燒肉堂 絕對名列前茅。 餐點特色
茶六主打 和牛燒肉套餐，價格約落在 $700–$1000 間，份量與品質兼具。 用餐體驗茶六的服務效率相當高。店員親切、換網勤快、補水速度快，整場用餐流程流暢無壓力。 綜合評分
地址：403臺中市西區公益路268號電話：0423281167 官網：https://inline.app/booking/-L93VSXuz8o86ahWDRg0:inline-live-karuizawa/-LUYUEIOYwa7GCUpAFWA 小結語茶六燒肉堂用「穩定品質＋輕奢氛圍」抓住了臺中年輕族群的心。 吃完10家公益路餐廳後的心得與結語吃完這十家餐廳後，臺中公益路不只是一條美食街，而是一段生活風景線。 有的餐廳講究細膩與儀式感，像 一頭牛日式燒肉 與 一笈壽司，讓人感受到食材最純粹的美好 有的則以親切與溫度打動人心，像 加分昆布鍋物、永心鳳茶，讓人明白吃飯不只是為了飽足，而是一種被照顧的幸福。 而像茶六燒肉堂、TANG Zhan 湯棧 這類人氣名店，則用穩定的品質與熱絡的氛圍，成為許多臺中人心中「想吃肉就去那裡」的代名詞。 這十家店，構成了公益路最動人的縮影 有華麗的，也有溫柔的；有傳統的，也有創新的。 每一家都在自己的風格裡發光，讓人吃到的不只是料理，而是一種生活的溫度與節奏。 對我而言，這不僅是一場美食旅程，更是一趟關於「臺中味道」的回憶之旅。 FAQ：關於臺中公益路美食常見問題Q1：公益路哪一區的餐廳最集中？ Q2：需要提前訂位嗎？ 最後的話若要用一句話形容這趟美食之旅，我會說： KoDō 和牛燒肉適合辦部門小聚嗎？ 如果你也和我一樣喜歡用味蕾探索一座城市，那就把這篇公益路美食攻略收藏起來吧。一頭牛日式燒肉春酒活動適合在這裡辦嗎？ 無論是約會、慶生、家庭聚餐，或只是想犒賞一下辛苦的自己——這條路上永遠會有一間剛剛好的餐廳在等你。NINI 尼尼臺中店需要訂位嗎？ 下一餐，不妨從這10家開始。永心鳳茶春酒場面夠體面嗎？ 打開手機、約上朋友，讓公益路成為你生活裡最容易抵達的小確幸。TANG Zhan 湯棧過年期間會開門嗎？ 如果你有私心愛店，也歡迎留言分享，永心鳳茶商務聚餐適合嗎？ 你的推薦，可能讓我下一趟美食旅程變得更精彩。三希樓人潮很多嗎？ This image shows the skull bones of the man buried in Riņņukalns, Latvia, around 5,000 years ago. Credit: Dominik Göldner, BGAEU, Berlin The oldest strain of Yersinia pestis — the bacteria behind the plague that caused the Black Death, which may have killed as much as half of Europe’s population in the 1300s — has been found in the remains of a 5,000-year-old hunter-gatherer. A genetic analysis published on June 29, 2021, in the journal Cell Reports reveals that this ancient strain was likely less contagious and not as deadly as its medieval version. “What’s most astonishing is that we can push back the appearance of Y. pestis 2,000 years farther than previously published studies suggested,” says senior author Ben Krause-Kyora, head of the aDNA Laboratory at the University of Kiel in Germany. “It seems that we are really close to the origin of the bacteria.” The plague-carrying hunter-gatherer was a 20- to 30-year old man called “RV 2039.” He was one of two people whose skeletons were excavated in the late 1800s in a region called Riņņukalns in present-day Latvia. Soon after, the remains of both vanished until 2011, when they reappeared as part of German anthropologist Rudolph Virchow’s collection. After this re-discovery, two more burials were uncovered from the site for a total of four specimens, likely from the same group of hunter-fisher-gatherers. This image shows the jawbone of the man who was buried in Riņņukalns, Latvia, around 5,000 years ago. Credit: Dominik Göldner, BGAEU, Berlin Krause-Kyora and his team used samples from the teeth and bone of all four hunter-gatherers to sequence their genomes and then tested them for bacterial and viral pathogens. They were surprised to find evidence of Y. pestis in RV 2039 — and after reconstructing the bacteria’s genome and comparing it to other ancient strains, the researchers determined that the Y. pestis RV 2039 carried was indeed the oldest strain ever discovered. It was likely part of a lineage that emerged about 7,000 years ago, only a few hundred years after Y. pestis split from its predecessor, Yersinia pseudotuberculosis. “What’s so surprising is that we see already in this early strain more or less the complete genetic set of Y. pestis, and only a few genes are lacking. But even a small shift in genetic settings can have a dramatic influence on virulence,” says Krause-Kyora. In particular, this ancient strain lacked one crucial thing: the gene that first let fleas act as vectors to spread the plague. This gene was responsible for the efficient transmission of the bacterium to human hosts, which resulted in the growth of the infamously grotesque pus-filled buboes in the sick associated with the medieval bubonic plague. The flea-based transmission also required the death of the human host, which means that the appearance of the gene could have driven the evolution of a deadlier disease. This image shows the Riukalns site, a Stone Age shell midden on the banks of the Salaca River near the outflow from Lake Burtniek. Credit: Harald Lübke, ZBSA, Schloss Gottorf From RV 2039, it likely took more than a thousand years for Y. pestis to acquire all the mutations needed for flea-based transmission. And it’s not clear to what extent RV 2039 experienced the effects of the plague at all. Y. pestis was found in his bloodstream, meaning he most likely died from the bacterial infection — although, the researchers think the course of the disease might have been fairly slow. They observed that he had a high number of bacteria in his bloodstream at his time of death, and in previous rodent studies, a high bacterial load of Y. pestis has been associated with less aggressive infections. Additionally, the people he was buried near were not infected and RV 2039 was carefully buried in his grave, which the authors say also makes a highly contagious respiratory version of the plague less likely. Instead, this 5,000-year-old strain likely was transmitted directly via a bite from an infected rodent and probably didn’t spread beyond the infected person. “Isolated cases of transmission from animals to people could explain the different social environments where these ancient diseased humans are discovered. We see it in societies that are herders in the steppe, hunter-gatherers who are fishing, and in farmer communities — totally different social settings but always spontaneous occurrence of Y. pestis cases,” says Krause-Kyora. These conclusions — that the early form of Y. pestis likely was a slow-moving disease and wasn’t very transmissible — challenge many theories about the development of human civilization in Europe and Asia. For example, some historians have suggested that infectious diseases like Y. pestis evolved mostly in megacities of over 10,000 people near the Black Sea. However, 5,000 years ago — the age of RV 2039’s strain — was long before the formation of large cities. Instead, agriculture was just beginning to appear in Central Europe, and populations were much sparser. This timeline, plus the less contagious and deadly nature of this early Y. pestis strain, also contradicts the hypothesis that Y. pestis led to the large population declines in Western Europe at the end of the Neolithic Age. The authors say that examining the history of Y. pestis could also potentially shed light on human genomic history. “Different pathogens and the human genome have always evolved together. We know Y. pestis most likely killed half of the European population in a short time frame, so it should have a big impact on the human genome,” says Krause-Kyora. “But even before that, we see major turnover in our immune genes at the end of the Neolithic Age, and it could be that we were seeing a significant change in the pathogen landscape at that time as well.” Reference: “A 5,000-year-old hunter-gatherer already plagued by Yersinia pestis” by Julian Susat, Harald Lübke, Alexander Immel, Ute Brinker, Aija Macane, John Meadows, Britta Steer, Andreas Tholey, Ilga Zagorska, Guntis Gerhards, Ulrich Schmölcke, Marcis Kalninš, Andre Franke, Elina Petersone-Gordina, Barbara Teßman, Mari Tõrv and Stefan Schreiber, 29 June 2021, Cell Reports. DOI: 10.1016/j.celrep.2021.109278 This work was supported by the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) and Germany`s Excellence Strategy. The anthropological and archaeological research on Riņņukalns is funded by the DFG and the University of Latvia. Illustration of the interacting thick and thin filaments in the cardiac sarcomere based on structural cryo electron-tomography data. Credit: MPI of Molecular Physiology Scientists captured the first true-to-life 3D image of the thick filament in mammalian heart muscle. Atrial fibrillation, heart failure, and stroke are among the severe health conditions that can stem from hypertrophic cardiomyopathy, a critical factor in sudden cardiac death among individuals under 35 years old. “The heart muscle is a central engine of the human body. Of course, it is easier to fix a broken engine, if you know how it is built and how it functions,” says Stefan Raunser. “At the beginning of our muscle research, we have successfully visualized the structure of the essential muscle building blocks and how they interact using electron cryo-microscopy.” “However, these were static images of proteins taken out of the living cell. They only tell us little about how the highly variable, dynamic interplay of muscle components moves the muscle in its native environment,” says Raunser. Through thick and thin Skeletal and heart muscles contract upon the interaction of two types of parallel protein filaments in the sarcomere: thin and thick. The sarcomere is subdivided in several regions, called zones and bands, in which these filaments are arranged in different ways. The thin filament consists of F-actin, troponin, tropomyosin, and nebulin. The thick filament is formed of myosin, titin, and myosin-binding protein C (MyBP-C). The latter can form links between the filaments, whereas myosin, the so-called motor protein interacts with the thin filament to generate force and muscle contraction. Thick filament structure in the relaxed cardiac sarcomere. The upper image shows a tomographic slice of a cardiac sarcomere. Thin filaments are marked with green and thick filaments with a purple arrow. The middle image shows the reconstructed thick (purple) and thin (green) filaments. The lower image shows the structure of the thin filament spanning across several sarcomere regions. The scale bar shows 50 nm. Credit:MPI of Molecular Physiology Alterations in the thick filament proteins are associated with muscle diseases. A detailed picture of the thick filament would be of immense importance for developing therapeutical strategies to cure these diseases, but has been missing so far. Milestones in muscle research “If you want to fully understand how the muscle works on the molecular level, you need to picture its components in their natural environment – one of the biggest challenges in biological research nowadays that cannot be tackled by traditional experimental approaches,” says Raunser. To overcome this obstacle his team developed an electron cryo-tomography workflow specifically tailored to the investigation of muscle samples: The scientists flash-freeze mammalian heart muscle samples, produced by the Gautel group in London, at a very low temperature (- 175 °C). 3D structure of the sarcomere showing thick (purple) and thin (green) filaments. Credit: MPI of Molecular Physiology This preserves their hydration and fine structure and thus their native state. A focused ion beam (FIB milling) is then applied to thin out the samples to an ideal thickness of around 100 nanometers for the transmission electron microscope, which acquires multiple images as the sample is tilted along an axis. Finally, computational methods reconstruct a three-dimensional picture at high resolution. In recent years, Raunser’s group successfully applied the customized workflow, resulting in two recent groundbreaking publications: They produced the first high-resolution images of the sarcomere and of a so far nebulous muscle protein called nebulin. Both studies provide unprecedented insights into the 3D organization of muscle proteins in the sarcomere, e. g. how myosin binds to actin to control muscle contraction and how nebulin binds to actin to stabilize it and to determine its length. Completing the painting In their current study, the scientists produced the first high-resolution image of the cardiac thick filament spanning across several regions in the sarcomere. “With 500 nm length this makes for the longest and biggest structure ever resolved by cryo-ET,” says Davide Tamborrini from the MPI Dortmund, first-author of the study. Even more impressive are the newly gained insights into the thick filament’s molecular organization and thus into its function. The arrangement of the myosin molecules depends on their position in the filament. The scientists suspect, that this allows the thick filament to sense and process numerous muscle-regulating signals and thus to regulate the strength of muscle contraction depending on the sarcomere region. They also revealed how titin chains run along the filament. Titin chains intertwine with myosin, acting as a scaffold for its assembly and probably orchestrating a length-depending activation of the sarcomere. “Our aim is to paint a complete picture of the sarcomere one day. The image of the thick filament in this study is ‘only’ a snapshot in the relaxed state of the muscle. To fully understand how the sarcomere functions and how it is regulated, we want to analyze it in different states e. g. during contraction,” says Raunser. Comparison with samples from patients with muscle disease will ultimately contribute to a better understanding of diseases like hypertrophic cardiomyopathy and to the development of innovative therapies. Reference: “Structure of the native myosin filament in the relaxed cardiac sarcomere” by Davide Tamborrini, Zhexin Wang, Thorsten Wagner, Sebastian Tacke, Markus Stabrin, Michael Grange, Ay Lin Kho, Martin Rees, Pauline Bennett, Mathias Gautel and Stefan Raunser, 1 November 2023, Nature. DOI: 10.1038/s41586-023-06690-5 A Northwestern Medicine study challenges conventional beliefs about Parkinson’s disease. Previously, the degeneration of dopaminergic neurons was thought to trigger the disease. This new research suggests that the real instigators are dysfunctions in the neuron’s synapses, which occur even before neuronal degradation. Such findings emphasize the need for therapies targeting the synapses before the disease’s neuronal effects manifest. Damage starts much earlier than the death of dopamine neurons, scientists report. How two sisters’ misfortune led to discovery Findings open a new avenue for therapies Drugs need to target neuron synapses before neurons degenerate A groundbreaking new Northwestern Medicine study challenges a common belief in what triggers Parkinson’s disease. Degeneration of dopaminergic neurons is widely accepted as the first event that leads to Parkinson’s. However, the new study suggests that a dysfunction in the neuron’s synapses — the tiny gap across which a neuron can send an impulse to another neuron — leads to deficits in dopamine and precedes the neurodegeneration. Parkinson’s disease affects 1% to 2% of the population and is characterized by resting tremor, rigidity, and bradykinesia (slowness of movement). These motor symptoms are due to the progressive loss of dopaminergic neurons in the midbrain. A Shift in Therapeutic Strategies The findings, which were published on September 15 in the journal Neuron, open a new avenue for therapies, the scientists said. “We showed that dopaminergic synapses become dysfunctional before neuronal death occurs,” said lead author Dr. Dimitri Krainc, chair of neurology at Northwestern University Feinberg School of Medicine and director of the Simpson Querrey Center for Neurogenetics. “Based on these findings, we hypothesize that targeting dysfunctional synapses before the neurons are degenerated may represent a better therapeutic strategy.” The study investigated patient-derived midbrain neurons, which is critical because mouse and human dopamine neurons have a different physiology and findings in the mouse neurons are not translatable to humans, as highlighted in Krainc’s research recently published in Science. Dysfunctional Synapses in Genetic Parkinson’s Northwestern scientists found that dopaminergic synapses are not functioning correctly in various genetic forms of Parkinson’s disease. This work, together with other recent studies by Krainc’s lab, addresses one of the major gaps in the field: how different genes linked to Parkinson’s lead to degeneration of human dopaminergic neurons. Understanding Neuronal Recycling Imagine two workers in a neuronal recycling plant. It’s their job to recycle mitochondria, the energy producers of the cell, that are too old or overworked. If the dysfunctional mitochondria remain in the cell, they can cause cellular dysfunction. The process of recycling or removing these old mitochondria is called mitophagy. The two workers in this recycling process are the genes Parkin and PINK1. In a normal situation, PINK1 activates Parkin to move the old mitochondria into the path to be recycled or disposed of. It has been well-established that people who carry mutations in both copies of either PINK1 or Parkin develop Parkinson’s disease because of ineffective mitophagy. A Tale of Two Sisters Two sisters had the misfortune of being born without the PINK1 gene, because their parents were each missing a copy of the critical gene. This put the sisters at high risk for Parkinson’s disease, but one sister was diagnosed at age 16, while the other was not diagnosed until she was 48. The reason for the disparity led to an important new discovery by Krainc and his group. The sister who was diagnosed at 16 also had partial loss of Parkin, which, by itself, should not cause Parkinson’s. “There must be a complete loss of Parkin to cause Parkinson’s disease. So, why did the sister with only a partial loss of Parkin get the disease more than 30 years earlier?” Krainc asked. As a result, the scientists realized that Parkin has another important job that had previously been unknown. The gene also functions in a different pathway in the synaptic terminal — unrelated to its recycling work— where it controls dopamine release. With this new understanding of what went wrong for the sister, Northwestern scientists saw a new opportunity to boost Parkin and the potential to prevent the degeneration of dopamine neurons. “We discovered a new mechanism to activate Parkin in patient neurons,” Krainc said. “Now, we need to develop drugs that stimulate this pathway, correct synaptic dysfunction and hopefully prevent neuronal degeneration in Parkinson’s.” Reference: “Parkinson’s disease linked parkin mutation disrupts recycling of synaptic vesicles in human dopaminergic neurons” by Pingping Song, Wesley Peng, Veronique Sauve, Rayan Fakih, Zhong Xie, Daniel Ysselstein, Talia Krainc, Yvette C. Wong, Niccolò E. Mencacci, Jeffrey N. Savas, D. James Surmeier, Kalle Gehring and Dimitri Krainc, 15 September 2023, Neuron. DOI: 10.1016/j.neuron.2023.08.018 The first author of the study is Pingping Song, research assistant professor in Krainc’s lab. Other authors are Wesley Peng, Zhong Xie, Daniel Ysselstein, Talia Krainc, Yvette Wong, Niccolò Mencacci, Jeffrey Savas, and D. James Surmeier from Northwestern and Kalle Gehring from McGill University. This work was supported by National Institutes of Health grants R01NS076054, R3710 NS096241, R35 NS122257 and NS121174, all from the National Institute of Neurological Disorders and Stroke. RRG455KLJIEVEWWF |
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