Symptoms<\/p>\n
The word \u201caphasia\u201d means a language disorder caused by brain damage, but there are different types of aphasia. Firstly, there is \u201clogopenic\u201d aphasia, which is an atypical form of Alzheimer\u2019s disease where people have difficulties with searching for the right word<\/a>, although their ability to physically produce speech is not affected.<\/p>\n These word-finding difficulties can lead to long pauses in conversations. People with logopenic aphasia can also get parts of words muddled up, for instance saying \u201caminal\u201d instead of \u201canimal\u201d.<\/p>\n More unusually, semantic dementia, which is a form of FTD, affects a person\u2019s \u201csemantic memory\u201d, their knowledge-store of what objects are, and what words mean. If you said to somebody with semantic dementia \u201cWhat did you have for breakfast?\u201d they might say: \u201cWhat\u2019s breakfast?\u201d People with semantic dementia can speak quite fluently \u2013 but they may seem to use more general words, such as \u201cthingy\u201d.<\/p>\n There is a third type of aphasia known as progressive non-fluent aphasia, also a type of FTD, where a person has problems speaking, constructing sentences and using grammar. Their speech might sound very slow or physically difficult, or they may get the order of words in a sentence mixed up. Difficulties with word order and sentences can be present in writing as well as speech.<\/p>\n If you suspect a family member has PPA, a specialist will examine progressive language decline, plus a neurological examination, neuropsychological testing for language and cognition, and brain imaging.<\/p>\n Treatment<\/p>\n Speech and language therapy can help in the early stages. As logopenic aphasia is typically caused by the plaques and tangles of Alzheimer\u2019s disease, people could benefit from future Alzheimer\u2019s drugs.<\/p>\n 4. Posterior cortical atrophy (PCA, or Benson\u2019s syndrome)<\/p>\n PCA literally means back of the brain shrinkage, which results in visual problems seeing what and where things are. This is an issue with \u201cbrain sight\u201d, not \u201ceyesight\u201d \u2013 the information from their eyes is transmitted, but gets misinterpreted. The most common cause of PCA \u2013 in more than 90 per cent of cases \u2013 is Alzheimer\u2019s disease, but for reasons we don\u2019t yet fully understand, the disease targets the visual networks at the back of the brain rather than the memory networks at the sides first.<\/p>\n Symptoms<\/p>\n A person in their 40s might go to the doctor and say: \u201cI can\u2019t see properly.\u201d The GP thinks they are too young for dementia, so the patient gets sent to the ophthalmologist. They will try loads of glasses but none of them work.<\/p>\n For example, we once met a gentleman with PCA in his 50s whose first symptom was having difficulty playing badminton. Strikingly, he could see the shuttlecock when it was moving during the rally, but couldn\u2019t find it when it was stationary on the floor. We determined that he had this form of Alzheimer\u2019s that affects the visual centres in the back of the brain.<\/p>\n Many others describe having difficulties with driving and parallel parking. Memory is relatively preserved in PCA. The average age of diagnosis with PCA is 58, but the youngest person I\u2019ve seen was 25.<\/p>\n Treatment<\/p>\n For the majority where Alzheimer\u2019s disease is the underlying cause, existing and new symptomatic and disease-modifying treatments should be beneficial.<\/p>\n 5. Familial Alzheimer\u2019s disease<\/p>\n A small proportion of those with Alzheimer\u2019s \u2013 fewer than 1 per cent \u2013 have a form that is directly inherited, with children of someone with the gene mutation<\/a> having a 50:50 chance of inheriting the gene and almost certainly developing the condition if they do. Symptoms can start in a person\u2019s 30s, 40s or 50s.<\/p>\n Symptoms<\/p>\n As with typical Alzheimer\u2019s disease, the first symptoms tend to be memory loss alongside new difficulties with planning or performing calculations emerging as the disease spreads.<\/p>\n Treatment<\/p>\n A diagnosis of FAD comes with extra burdens: those at risk may be caring for a relative when they find out, and may need to access specialist genetic counselling and support.<\/p>\n Many of our research trials involve these incredible people \u2013 this work is vital as we can test potential treatments before damage has occurred in the brain and symptoms emerge to determine whether the underlying disease might be slowed.<\/p>\n 6. Lewy body dementia (LBD)<\/p>\n This is an umbrella term that includes dementia with Lewy bodies<\/a> and Parkinson\u2019s disease dementia.<\/p>\n LBD is caused by a build-up of proteins called \u201cLewy bodies\u201d in the brain. Lewy body dementia may account for up to10 per cent of all dementia and is typically a later-onset condition, after the age of 65.<\/p>\n Symptoms<\/p>\n LBD can affect thinking and memory, and also cause visual hallucinations<\/a> \u2013 seeing things that are not there such as children and small animals \u2013 as well as movement changes similar to Parkinson\u2019s disease such as slowness, stiffness and tremors. People with LBD also experience cognitive fluctuations, with memory and thinking difficulties varying<\/a> from day to day or even hour to hour.<\/p>\n Treatment<\/p>\n Dementia drugs such as cholinesterase inhibitors are used to manage cognitive symptoms. Levodopa \u2013 a Parkinson\u2019s medication \u2013 can help manage motor symptoms, whilst clinical trials are looking for new treatments to slow the progression of LBD.<\/p>\n As told to Miranda Levy<\/p>\n