Alzheimers medicin 2023

Af Madeleine Darling Sagmo

I USA har sundhedsmyndighederne netop godkendt medikamentet Leqembi (lecanemab), som er en ny slags medicin mod Alzheimers sygdom. Medicinen kan ifølge studier bremse svækkelsen af hukommelse og tænkning hos patienter med milde symptomer med 27 procent over en periode på 18 måneder.

Det er ifølge Alzheimerforeningens direktør, Nis Peter Nissen, en positiv nyhed. Det er dog vigtigt at påpege, at medicinen ikke kan stoppe sygdommen. Medicinen skal først og fremmest bruges på patienter, som står i den tidlige fase af Alzheimers sygdom og som derfor kun har milde symptomer. Forskningsresultaterne viser, at medicinen kan forsinke sygdommen og give et bedre funktionsniveau, sammenlignet med hvis man ikke tager medicinen.

Opråb og wakeupcall til regeringen

Hvis Leqembi bliver godkendt i Danmark, er det ifølge Nis Peter Nissen vigtigt, at regeringen opruster det danske sundhedsvæsen og tager fat om de allerede markante udfordringer med lange ventelister til at blive udredt. For da medicinen særligt gavner mennesker i den tidlige fase af Alzheimers sygdom, kræver det også et øget fokus på at opspore og udrede sygdommen.

Selvom der for dem

Clinical trials of new drugs for Alzheimer disease: a – update

Alzheimer disease (AD) represents a major global medical, social, and economic burden. The World Alzheimer Report revealed that more than 55 million people have AD or related conditions worldwide, and this number is projected to reach 82 million by and million by [1]. Typically, AD first manifests as progressive memory decline accompanied or followed by other cognitive dysfunctions, such as visuospatial abnormalities, navigation difficulties, executive problems, and language disturbances. These cognitive impairments affect the performance of activities of daily living. During the course of AD, many behavioral and psychological symptoms of dementia (BPSD) occur [2,3,4].

Although the exact causes of AD remain unclear, the disease has two pathological hallmarks: plaques composed of amyloid-beta (Aβ) fibrils and neurofibrillary tangles (NFTs) consisting of hyperphosphorylated tau protein [5,6,7]. The key event in AD pathogenesis is believed to be Aβ accumulation. Cerebral Aβ fibril deposition may occur decades before the onset of clinical symptoms [8]. Brain atrophy, particularly in the hippocampus, is major indicator

Start of new era for Alzheimer’s treatment

Researchers säga we appear to be at the start of a new era for Alzheimer’s treatment. Trial results published in January showed that for the first time a drug has been able to slow the cognitive decline characteristic of the disease. The drug, lecanemab, is a monoclonal antibody that works by binding to a key protein linked to the malady, called amyloid-beta, and removing it from the body. Experts säga the results offer hope that the slow, inexorable loss of memory and eventual death brought bygd Alzheimer’s may one day be a thing of the past.

The Gazette spoke with Scott McGinnis, an assistant professor of neurology at Harvard Medical School and Alzheimer’s disease specialist at Brigham and Women’s Hospital, about the results and a new clinical trial testing whether the same drug given even earlier can prevent its progression.

Q&A

Scott McGinnis

GAZETTE: The results of the Clarity AD trial have some saying we’ve entered a new era in Alzheimer’s treatment. Do you agree?

McGINNIS: It’s appropriate to consider it a new era in Alzheimer’s treatment. Until we obtained the results of this study, trials suggested that the only mode