About dementia and neurodegeneration
While there has been substantial progress in treatment of cancer and cardiovascular diseases the last decades, neurological disorders are increasing societal challenges.
For example, due to an aging population, the prevalence of dementia is expected to double every 20 years and reach 130 million people worldwide by 2050.
Below are some of the diseases that we are studying at the Division for Neurogeriatrics:
Alzheimer Disease (AD) is the most common form of dementia. The prevalence of AD is around 1% at age 65 and 20% after 85 years. The disease affects cognitive functions such as memory but can also result in changes of mood, disorientation in time and space and at later stages deterioration of language and motor abilities. Apart from age, risk factors for AD include increasing genetic factors, female gender, low education, hypertension and head trauma. A small proportion of the disease is purely familial and inherited in a direct manner. There is currently no preventative or curative treatment available, although there are a number of drugs that can provide certain symptomatic relief. At the Department of Neurobiology, Care Sciences and Society, several research groups investigate this disorder from different perspectives, emphasizing the integration of basic neuroscience, clinical research, molecular genetics and epidemiology.
Frontotemporal dementia (FTD) is a group of neurodegenerative diseases characterized by neuronal dysfunction in the anterior temporal lobes and frontal lobes. The clinical symptoms are characterized by behavioral changes and or language dysfunction. There is a clinical, genetic and neuropathological overlap with ALS (Amyotrophic lateral sclerosis). We investigate the genetics and neuropathology of FTD in both clinical studies of at-risk subjects as well as experimental studies of patient derived cells and fluids. We are partners of the international Genetic FTD initiative (genfi.org.uk) and we have recently initiated a National consortia called Swedish FTD Initiative (FTDemens.se).
CADASIL (cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy) is the most common familial form of small vessel disease. The condition leads to a series of increasingly severe strokes and dementia. CADASIL is linked to the Notch3 protein which is an important signaling protein allowing cells to communicate with one another. Mutations in the NOTCH3 gene result in misfolded Notch3 accumulating around small and middle-sized arteries throughout the body. At present how these Notch3 deposits affect the surrounding tissues is unclear. The disease mechanisms may be further complicated due to altered Notch3 signalling. A number of genetic disorders such as familial Alzheimerdisease are directly linked to protein misfolding, which strongly suggest that abnormal protein accumulation and deposits play a direct cytotoxic role in the disease.
Spinal cord injury
Spinal cord injury causes loss of mobility and sensation below the lesion, affect the control of bowel, bladder and sexual functions, as well as often result in altered regulation of blood pressure and other general functions. Some spontaneous improvement may occur after the injury, however functional impairment is today often life-long. There is currently no established clinical treatment to replace lost nervous tissue.
Medical experimental research focus on reducing the spreading of the acute damage, stimulating regrowth of nerve fibers, restoring lost nerve tissue by transplanting immature neural cells, and controlling paralyzed muscles and organs through electronic devices. Considerable progress has been made, but more research is necessary to repair damaged neural pathways to regain lost functions after spinal cord injury.