எங்கள் குழு ஒவ்வொரு ஆண்டும் அமெரிக்கா, ஐரோப்பா மற்றும் ஆசியா முழுவதும் 1000 அறிவியல் சங்கங்களின் ஆதரவுடன் 3000+ உலகளாவிய மாநாட்டுத் தொடர் நிகழ்வுகளை ஏற்பாடு செய்து 700+ திறந்த அணுகல் இதழ்களை வெளியிடுகிறது, இதில் 50000 க்கும் மேற்பட்ட தலைசிறந்த ஆளுமைகள், புகழ்பெற்ற விஞ்ஞானிகள் ஆசிரியர் குழு உறுப்பினர்களாக உள்ளனர்.
அதிக வாசகர்கள் மற்றும் மேற்கோள்களைப் பெறும் திறந்த அணுகல் இதழ்கள்
700 இதழ்கள் மற்றும் 15,000,000 வாசகர்கள் ஒவ்வொரு பத்திரிகையும் 25,000+ வாசகர்களைப் பெறுகிறது
Armin Von Gunten, Marie-thérèse Clerc, Rahul Tomar and Paul St John-Smith
Increasingly people are surviving into old age both in high and middle/low income countries. The increase in longevity is associated with increased levels of morbidity of both somatic and mental disorders during those added years. These pathologies prompt developing strategies for effective prediction, prevention and treatment of such disorders, among them the dementias such as Alzheimer’s disease (AD). Aging lies on a temporal continuum that starts at conception and ends at death. It refers to the aging processes occurring during an individual’s lifetime. However, our understanding of aging remains limited. In the early stages of dementia, distinguishing normal from pathological aging remains complex. Medical research customarily investigates the immediate mechanisms or pathogenesis of “how” diseases come about and affect patients. Evolutionary perspectives consider the reasons “why” people may have become particularly vulnerable to different conditions. Examining why people age is illuminating. Around the question whether aging is adaptive, we consider some evolutionary concepts useful around aging theories, among others antagonistic pleiotropy and life history theory and more recent concepts including evolvability and evolutionary developmental biology. As AD seems to be specific to homo sapiens, its existence may in part be anchored in the adaptive changes that have occurred after the hominidae separated from the pongidae. Around the question why apparently non-adaptive conditions such as AD are so frequent, we consider, among other aspects, brain development including the related phenomena of altriciality and grandmothering, the evolution of ApoE and the genome lag hypothesis. We consider the idea that the neuropathological hallmarks of AD help mitigate neurodegeneration and cognitive decline rather than being its cause. Thus, an evolutionary look into AD may shed new light on the currently still sombre perspectives regarding disease-modifying treatments of AD and prove useful as a root cause analysis.