The most commonly utilized treatments for semantic dementia are cholinesterase inhibitors and memantine. These medications enhance cholinergic and NMDA functioning, respectively, and thus potentially improve functioning in semantic dementia.
The data obtained from a cohort of individuals over 40 years of age suggests that PDD subjects have a very low level of disease progression over time. The finding that the patients from whom this study was drawn were over 40 years of age and had a slow or no progression would be expected in patients with AD but not in patients with other dementing diseases. Although semantics remains a controversial entity in neurodegenerative disorders that cause clinical dementia, the data support the assertion that semantics can be lost but can be rehabilitated in AD, and that semantic dementia can thus be cured.
Semantic dementia can present with symptoms similar to those of multiple neurodegenerative disorders, so a clinical history and neurologic examination are essential in order to reach the correct diagnosis.
Semantic dementia is now known as semantic language disorder. It is the result of damage in a specific area of the brain—the left inferior frontal gyrus—which has been associated with abnormal semantic comprehension and production of word meanings, particularly names. In some respects, individuals with semantic dementia resemble individuals with Alzheimer's disease. The clinical and pathological profiles of semantic dementia are almost identical with those in semantic pragmatic disorder, a neuropsychological disorder associated with damage to the anterior inferior frontal gyrus in right hemisphere patients. While semantic language disorder is still a relatively unknown and undefined disorder in the current diagnostic manuals, accumulating evidence based on imaging and neuropsychological testing (especially of the right hemisphere) supports the diagnosis of semantic dementia.
Around 1.9 million Americans are diagnosed with semantic dementia each year, making it the fourth most common dementia among people over the age of 60. At least 1 million of these cases probably represent undiagnosed cases. Patients with semantic dementia often present with late onset, progressive and chronic cognitive impairment. These patients often experience memory loss, deficits in language and other aspects of semantic knowledge and comprehension. In the United States, approximately 40,000 Medicare members die each year either from semantic dementia or from the dementia of Alzheimer's disease. Semantic dementia was included as a major reason for admission to nursing homes for Medicare beneficiaries in 2003, which suggests it causes considerable resource expenditure.
The common theory of semantic dementia is that language deterioration is caused by a loss of semantic networks, mainly involving semantic fluency. Results from a recent clinical trial suggest that semantic dementia is not a memory deficit disease.
The recent progress in our understanding of the mechanism of lithium's antipsychotic effect allows researchers to develop novel treatments based on lithium's actions. One such treatment being researched is the possible combination of lithium and sodium-glucose cotransport inhibitors (SGLT1 inhibitors). The combination of a SGLT1 inhibitor and lithium can inhibit neuronal cell death thought to be the cause of schizophrenia and bipolar disorder. Lithium and its use in treating schizophrenia and bipolar disorder has been criticized for over 140 years. This new treatment will probably prove effective in patients with those conditions.
Results from a recent clinical trial from this analysis reveal that the primary cause of semantic dementia is vascular/degenerative dementia and not an infiltrative type of dementia.
In addition to semantic dementia, there is evidence that Alzheimer's, Parkinson's and Lewy body dementia are increasingly diagnosed in the health system. As researchers continue to develop and test the potential of AD/DLB and PD treatments, the rate of these diagnoses will surely increase. There is considerable evidence of some efficacy and safety of existing treatments.
Clinical trials for semantic dementia do not seem to benefit those who are already symptomatic, but may benefit those who are mildly cognitively impaired. Therefore, most adults with symptoms suggestive of semantic dementia should be referred to clinical trials in order to reduce the number of people with semantic dementia who die without ever being properly evaluated for a potential trial.
Severe adverse events from lithium carbonate treatment are extremely rare. This is in contrast to the more common adverse effects of lithium bromide, such as hypertriglyceridemia, hyperprolactinemia, and tremor, which tend to be mild. Thus, the data suggest that lithium carbonate is a more well-tolerated adjunct to cognitive behavioral therapy (CBT) than lithium bromide. At the same time, there is a potential for mild hypothyroid symptoms, including weight gain and tremor, due to reduced insulin release (i.e. diabetes mellitus type 1).
Given the rarity of SemD and the familial mode of inheritance, our results, if confirmed, may be interpreted as supporting a genetic aetiology. However, this remains to be tested on a larger cohort of kindreds.